Q&A with Fred – Thyroid concerns in Labs
Hello,
I have a very serious problem occurring with one of my Labs. I came across your article “Thyroid Problems and Suggestions on Dealing with Them” this evening. It had some refreshingly different points of view and pieces of information. So, I am turning to you in the hope of receiving some useful help and advice. Continue reading
Front and Rear Angulation in the Working Dog
Dog breeds are grouped – often arbitrarily or erroneously – into from five to ten categories based on function, superficial appearance, or geographical origin, depending on the registry organization. Just because it may make more sense to assign them to groups based primarily on ancestry and then on historical function, does not mean that such will be the case. In most dog circles, the “working” breeds have always been considered as those that originally did such work as herding or guarding livestock, pulling loads, and protecting property. Even though other breeds had specific occupations in the service of man, they are not known as working breeds: sighthounds running down prey or predators, gundogs flushing food for the table, terriers and toys terrorizing vermin – these were more or less doing what they would do without human ownership, anyway, so their jobs were considered less like “work”.
Many dog organizations split the huge Working Group into two, with the ones that had historical development for tending, driving, or bunching flocks and herds being called “Herding breeds”. Never mind the confusion about whether the reindeer-herding Samoyed is hardly much different from the sled-pulling Husky – that’s a puzzle for another time. Most of the Group that did not resemble the mastino-type wagon puller or the bear-fighting wooly flock guardian type were once employed to trot around the animals raised by man for his food, and assigned to the herding subcategory. These latter were specialists in trotting, in covering much ground with the most efficiency (least effort). This meant that success favored those with the most shoulder angulation over those with the stiffer, more vertical front ends.
When we speak of a shoulder in a dog, we usually include a lot more than just the scapula (shoulder blade) – although the flat, broad bone is often the center of attention. No part of a dog exists alone, not even those “floating” bones such as the hyoid, sesamoid, clavicle, patella and penile bones, all of which are connected to muscles and other bones by ligaments and tendons. The shoulder is intimately related to most other portions of the foreassembly or “forequarters”, from the skull to the ribs, from vertebrae to arm and breastbone.
The scapula does not articulate with any bones at its top, but is attached by four muscles to the spinal column at a number of places from the first cervical to the ninth thoracic vertebra and to the first seven or eight ribs. This is the case whether the dog is steep-shouldered or well-laid back, so differences between the two types must be due to minor differences in scapula and humerus lengths and ratios; perhaps the lengths of the vertebrae; and the tightness and condition of the ligaments and muscles that hold the bones in their positions.
At the most forward and lowest portion of the scapula is a shallow socket in which articulates the head of the upper arm (humerus). This area, especially the humeral greater tubercle that protrudes in front of the articulation, is called the “point of the shoulder”. Running roughly up the center of the blade from that point nearly to the top is a ridge of bone known as the spine of the scapula. The lowest and thickest section of that spine close to the socket is the acromion. See Figure 2. There are several muscle groups attached to the scapula. Don’t be frightened by their names; use abbreviated nicknames if you stumble over pronunciation. What matters is that you know what action each gives to the blade and the entire limb, and where the muscles are attached.
The first of these is the triangular trapezius muscle originating on the bones and ligaments of the vertebral column from the third cervical (neck) vertebra to the ninth thoracic vertebrae. Its insertion is on the spine of the scapula. Since part of this thin broad muscle lies forward of the ridge it is attached to, and part extends to the rear, it can easily be seen that its function is primarily to elevate the limb. It also brings the arm forward and helps in changing the angle of layback during movement. The omotransversarius starts from the first cervical vertebra (the atlas) next to the back of the skull, dips beneath the other muscles of the neck, which extend to the sternum and arm, then attaches to the scapular spine near the acromion. Its obvious action is to draw the limb forward and rotate the bottom of the scapula forward while other muscles are trying to hold the rest of it in place. Knowing that, you can easily understand why a dog trotting in the show ring isn’t going to extend its forelimbs in ideal or equal reach if it has its head turned toward its handler. Nor will it cover as much ground if it trots with its head held high instead of forward and slightly above back level. Yet terrier and cocker dog-show handlers are notorious for the silly spectacle in which their dogs often barely touch the floor with their front paws!
Beneath the trapezius lies the rhomboideus muscle, which originates on the vertebrae from near the head to about the sixth or seventh thoracic vertebra. Its insertion is along the edge of the scapula, farthest from the acromion. Because of its wide origin, it can lift the limb upward, pull the limb and shoulder forward or backward and draw the scapula against the rib cage, depending on which portions are ennervated (stimulated by nerve impulses.)
The muscle filling the space in front of the scapular spine is called the supraspinatus, and it is attached to the top of the humerus. Thus, you can envision it straightening out the shoulder-arm angle and bringing the limb forward. The (behind the spine) will either flex or extend the shoulder joint, depending on the position when the muscle contracts. It also is inserted on the humerus. Other muscles include the infraspinatus, serratus, teres, deltoideus, and sub-scapularis; all play some parts in moving the scapula in relation to the ribs, vertebrae or upper arm.
Now that you have a little more understanding of the muscles and their actions on the bones, let’s get back to the subject of angulation. Some of what follows is similar to an excerpt from my book, The Total German Shepherd Dog.
The Front
Variously called the front assembly, forequarters, or shoulder, the whole combination made by the shoulder blade (scapula), upper arm (humerus), breastbone (sternum), and their related soft tissues is at the heart of much poor movement in dogs the world over.
Shoulder assembly – The least understood and most controversial portions of the AKC and most other Breed Standards relate to the angles proscribed for the forequarters and hindquarters. I disagree with the angles commonly reported to be ideal in the shoulder area, though much of the discrepancy may be a matter of how that angle is usually measured. To specify angles is useless unless exact points of reference are not only agreed upon but also easily determined. Since the bones forming these angles are curved, such “landmarks” as (1) the highest point of the scapula, (2) the foremost point of the upper arm where it meets the shoulder, and (3) the topmost point of the elbow should be used as well as a detailed illustration decided upon. Without X-ray vision, we need to rely on our fingers.
None of the editions or versions of the AKC Standard for the German Shepherd Dog has been sufficiently explanatory, nor have they been so in other breeds. Many years ago I radiographed standing dogs and found that what I had been reading in books and seeing in artists’ drawings was not true, even though I had already discovered that by digital palpation of bones and joints.
Many people hear and even use terms without a good understanding of their meanings. See my article on “topline” for another example of this. What is “shoulder layback?” Many dog fanciers are not sure. See Figure 1. It is the front-to-back inclination of the shoulder blade, seen and felt when one touches both the point of the shoulder and the top of the scapula or the withers at the same time. The withers is the area atop the shoulder from where the neck ends to where the “true back” begins. In most dogs, the last cervical vertebrae and the first thoracic vertebrae are down between the shoulder blades, so you might not be able to feel them, especially in well-muscled dogs. The withers is thus a transition stage between the neck’s relatively upright carriage and the nearly level back called for in most working breeds. (I use the term “working” in the utilitarian sense, and especially refer to the herding breeds.) The beginning judge (or the one evaluating heavily-coated breeds) often checks and compares layback by running his thumbs down the spine of the scapula. That line is almost parallel to, and only an inch or so behind, the envisioned line from the highest point of scapula to point of shoulder. Even so, among novices there is usually great disparity between what the fingers feel and what the mouth spouts!
In examining the standing dog, the good layback of 35 or 30 degrees can be determined either by feeling that line of the slope of the scapular spine, or by palpating those points mentioned above, and imagining a line between these points. These two sloping lines will be essentially parallel, so take your choice; in either case, you will have approached the question more scientifically. By observing the facts for yourself you will be able to arrive at a conclusion or hypothesis. The sooner we understand what is as opposed to what we imagine, the sooner we’ll understand how to get the most out of our dogs. Feeling that scapular spine is more difficult in a heavily muscled breed such as the Rottweiler.
The often-heard call for a 45-degree shoulder layback plus another supposed 45-degree angle to the “line” of the upper arm, equaling a 90-degree shoulder angle, is inaccurate and misleading. If lines are drawn on a radiograph or a sketch, along the scapular spine and down the center of the humerus as they usually are, a 90-degree angle in the real, live dog standing there before you will never be realized. Since the time I started challenging this notion, there have been noted authorities who have corroborated my claims with independent research, but it will be a long time before the old books are all revised and longer still before writers do their own investigative work instead of copying sketches from each other. One of the better drawings of the “ideal” (according to American tastes) German Shepherd Dog ever made in this country is Lloyd Fanning’s which appeared in the Review and in an early, small booklet on the breed published by the German Shepherd Dog Club of America. Strange, that so many have used incorrect representations instead of this fairly accurate sketch. An even better sketch is available from the SV and appears in many posters and magazines owned by those who appreciate the international (German) type.
If you draw your line (on a radiograph or in your mind) from point of shoulder to the highest part of the ulna that we call the point of the elbow (leaving the humerus to do so), you get points of reference you can see and feel. Now draw your second imaginary line from point of shoulder to top of shoulder blade. The angle between is closer to 90 degrees than if you tried to imagine and use a line going through the shaft of the humerus, but you still don’t get a right angle, even with the best laid-back shoulder blades. That touted right angle cannot be attained by drawing your lines down the middle of the upper arm on a radiograph. Whether or not you have x-ray vision, you will not be able to agree where a “center” line of this slightly curved, well-padded bone is!). In my live-dog illustrated lecture, “Analytical Approach to Evaluating Dogs”, I show where the lines can connect palpable points by drawing chalk lines on dark, short-coated canine volunteers. Even without using a protractor, my audiences can see the fallacies of those printed standard specifications. See Figures 1 and 4.
Sketches in my book on the breed represent the typical German Shepherd with a good shoulder. Dogs with better reach and a floating gait have close to the same angles and layback. I suspect much more credit for such gait lies in the muscles and ligaments than has been imagined, measured, or hinted at in the past. And of course, desire and drive make a big difference, too. In actuality, the ideal shoulder with an angle approaching that much-vaunted “90-degree” number (from point of elbow to point of shoulder to highest point on scapula) has about a 30 to 35-degree shoulder blade layback, not 45 degrees. Factors such as the relative lengths of scapula and humerus, the angle at which the humerus inclines, plus the dog’s attitude, play parts in both the standing appearance and in the reach in motion. While they didn’t have all the answers, Humphrey and Warner had most of them, and they determined that a scapula-humerus angle of 102° was ideal for the working German Shepherd Dog.
Another problem in reports of that fictitious 45° or greater layback is that it just doesn’t occur in the standing dog. Possibly you might exclude achondroplastic dwarf breeds such as the Corgi, although a noted Dachshund breeder once told me that my statement about “no such shoulder angle as 45 degrees” was true for his breed as well. It does happen when the dog is trotting, running, deeply crouching, or lying on its chest and belly in the manner of the Great Sphinx. The reason for this is that the scapula is not fixed or stationary; its lower end is pulled back by the trapezius and forward by the omotransversarius and serratus, with many other muscles being involved to a lesser extent. These angles can be visualized by watching slow-motion movies or the frames taken from those, and superimposing (technically, infra-imposing) the skeleton or lines representing the bones. Examining many dogs of varying qualities, hopefully with the guidance of a knowledgeable veteran, will enable you to see these proper angles in motion and in standing.
A very unfortunate situation has arisen out of ignorance and laziness: many AKC breed standards were written by people who copied the wording from other erroneous standards without checking accuracy first. The same problem is seen in the multitude of breed books in which artists’ drawings of canine skeletons could almost have been traced from other books, judging from the mistakes they have repeated.
I had been preaching scientific honesty and artistic accuracy for years, thinking I was, like Elijah, “the only prophet in the land of Baal” – until Rachel Page Elliot’s book Dogsteps came out. As I had done on a smaller scale, she x-rayed many standing and running dogs to prove the nonsense about 90 degree angles between humerus (upper arm) and scapula, and the impossibility of a 45-degree layback of the shoulder. That so-called right angle cannot even be approached if you draw your lines down the middle of the upper arm (if you have x-ray vision, maybe you can tell me where the “center” line of this slightly curved, well-padded bone is!).
The Bouvier’s AKC standard has quite good wording on this subject, as does the Collie’s. The “about a right angle” in the AKC German Shepherd Standard is misleading. Is slightly less as good as slightly more? Is it even possible? Their Doberman Pinscher standard is a travesty, what with the 45° layback and 90° shoulder/arm angles being specified. Might as well specify cubical tires for cars! And Dobes have a terrier-schnauzer-sighthound type of structure, with more “open” front angulation than in the herding breeds.
Why, within a particular breed, are some shoulder angles better than others? In a few cases this is the same as asking why some scapulas are laid back at a greater angle than others, though most deficiencies in front angulation lie in the upper arm rather than the scapula layback. If the angle of the spine of the scapula does indeed differ between dogs, it is possibly because some dogs have proportionately shorter vertebrae in the neck or sacrum, and some may have longer bones in the true back and loin (the true back being between the scapula and the croup). If the dog has shorter vertebrae and disks, the shoulder may more upright.
Use Your Fingers
If you draw your line from point of shoulder to the highest part of the ulna that we call the point of the elbow (leaving the humerus to do so), you get points of reference you can see and feel. Now draw your second imaginary line from point of shoulder to top of shoulder blade. The angle between is closer to 90 degrees than if you tried to use the line going through the shaft of the humerus, but you still don’t get a right angle, even with the best laid-back shoulder blades. In my live-dog illustrated lecture, “Analytical Approach to Evaluating Dogs”, I show where these lines are by drawing chalk lines on dark, short-coated canine volunteers. Even when I don’t use a protractor, my audiences can see the fallacies of those printed standard specifications. Again, see Figures 1 and 4.
Action and Motion
Remember that those trapezius and rhomboideus muscles extend to the ninth and sixth thoracic vertebrae with only a small portion of their fibers, and if the vertebrae are relatively short or the scapula is slightly more upright in that dog for another reason, the muscle attachment will be relatively forward and less broad. The same may be true to a lesser degree with the serratus ventralis, which runs from the scapula to the last five cervical vertebrae and the first seven ribs. The more forward all these attachments are, the less the blade will be inclined when a pup begins to move and muscle forces help shape its semi-cartilaginous bones and joints. In such a dog, there would be less muscle mass present to rotate the top of the scapula back and forth, thus a restriction of motion here contributes to a lack of reach in front and even follow-through beneath.
There is a far greater cause for poor reach, or less smoothness of front action. Some dogs have an upper arm (humerus) that is not laid back at a good angle from point of shoulder to elbow joint. This is sometimes accompanied by a proportionately shorter arm compared to the scapular length. Such dogs are in the minority, but it’s wise to keep an eye on the problem. Because of cyclic neglect, German Shepherd Dogs, have periodically become alternately better and worse in this respect. At the time of this revision, the AKC-GSDCA type has lacked good upper arm layback for many years while the international type has improved since the 1970s. See Figure 3 for one artist’s conception of ideal structure.
Whether herding livestock, doing police work, performing obedience exercises, or pulling loads, the working dog needs a well-angled shoulder/upper arm assembly. Let’s consider this synonymous with good layback of both bones, for convenience’s sake. A “straight” (more vertical) foreassembly is somewhat like a car without springs. Imagine a dog with poor front angulation hitting the ground with its forelimbs after climbing over a wall in pursuit of an errant lamb or thief. The hard shock will have a detrimental effect before long.
A dog with better angles (yet strong ligaments in pasterns, elbows, and shoulders) can spread that shock over an imperceptibly longer period of time, during which the muscles slow the impact while the bones go through their “folding up” action relative to each other, then release that stored energy by straightening out again (bouncing back). Trotting creates very nearly the same sort of shock that jumping does, only far less violent.
A successful parachutist survives because he takes only a tiny fraction of a second longer to hit the ground than someone whose chute didn’t open. A good boxer “rolls with the punches”, while the guy who holds his head still when the other guy’s fist approaches finds himself waking up some time later. The baseball player relies on padding and moving his hand back to slow the speed of the ball as it makes contact with his glove. The differences in time intervals in each illustration are truly minute, but they can mean the difference between ease and pain, or life and death. Likewise the differences in layback from dog to dog may be small, but a tiny difference can mean smoother action, greater ability to hit the ground effortlessly whether jumping or trotting, and a longer useful working life. The galloping breeds minimize that shock by increasing the horizontal-to-vertical motion ratio. My show champion, lure-coursing Whippet was undefeated after he learned to run “flat” instead of “up and down”. The trotter breeds have a little more need for more acute angles in the foreassembly.
Not many dogs are used for pulling loads anymore, but the dog with a smaller angle between scapula and upper arm is better suited for this type of work, too. Even if only for historical interest, the ability to pull carts or sleds should be preserved in those breeds that are developed for such purposes, for breed type is inextricably bound to that utility. Form follows function, and if we get too far in the evolution of breeds from their original purposes, we will have created (though gradually) a distinctly different breed. What time traveler from centuries past would recognize today’s utterly non-functional English Bulldog from those he had seen chase and tame wild bulls in the days when the breed had a useful purpose? Do not let our working, utilitarian breeds slip away into uselessness as some other breeds have. There is a good reason why I put so much emphasis on shoulder and upper arm angles, and reward good examples in the show ring. It’s the same reason why it is so difficult to improve in breeding.
Why is good front angulation harder to achieve and possibly more important?
In the case of angulation at the knee (“bend of stifle”), ignorance and fad-following have resulted in GSDs with lower-thighs that are too long, with hocks too far behind the torso to be adequately controlled by ligaments and muscles. This rear angulation at the stifle can go either direction from the middle (moderate) ideal for most breeds, with the American-fashion GSD at one extreme and Chows at the other. However, in the case of the shoulder, the ideal is not in the middle of a normal range, but on one end; namely, closer to the fictional 45-degree layback and 90-degree shoulder/arm angles. Actually, depending upon breed and whether you draw the bottom line to the point of the elbow, a layback of 35 degrees in either scapula or upper arm is very good, and an angle of 95 degrees from withers to point of shoulder to point of elbow is excellent for a herding breed. Drawing that line through the upper arm, you would get about 115 degrees in most of the efficient trotters. If it were possible to create a 45-degree layback in both bones, some say that such a dog might fall on its face.
But back to those palpable points of reference, those being the indentation at the point of shoulder, the highest point of the scapula, and the top of the ulna. If a number of genes affect the angle between these bones, some would be “ideal genes” (let’s say they’d call for a 35° angle from vertical, for each bone, for purpose of illustration), and others would be “less than ideal genes” calling for some lesser angle. Of all the possible genes that could be transmitted, the vast majority would be calling for an angle of somewhere in the 20 degree to 30 degree range, with a miniscule number calling for the coveted approximately 120 degrees remaining between the scapula and humerus. Genes are inherited randomly, and statistically would show a bell curve with the smallest amplitude in the two extremes (say, 15 degrees and 35 degrees, for example) and the greatest in the middle of the curve.
Despite all the talk about angles, it boils down to this advice: forget the numbers, examine as many dogs as you can get your hands and eyes on, compare one dog to the next, and reward or admire those with the smallest apparent angle between shoulder and upper arm, while proving what appears in stance by watching the dog perform in the trot. See Figures 4 and 5.
Since he cannot do “better” than the ideal shoulder angle, which is at one end of a range of possibilities, the breeder must be more diligent in such an instance to cull from breeding programs all dogs which drift an undesirable distance from that good end of that spectrum. More so than is necessary in any trait in which the ideal is at some intermediate point between the worst on one end and the worst in the opposite direction. In the case of good forequarter function in a herding breed, and in most other working breeds, there is only one direction from the ideal, when we speak of breeds developed for trotting. To paraphrase Sir Edmund Burke, eternal diligence is the price of freedom from poor forequarters.
The Hindquarters
The thigh – What is meant by “the whole assembly of the thigh” in the wording of the AKC Standard for the GSD? Viewed from the side, it includes the croup, upper thigh (femur and associated soft tissues), and lower thigh (tibia and fibula). If these three skeletal sections are too “vertical” or steep, the hindquarters will not present the broad picture called for by the Standard. Obviously, if the croup and lower thigh are slanted downward toward the rear, the femur will not also be so. Nor is it angled forward when the GSD stands in a normal pose, in spite of the AKC Standard’s inaccurate statement about it paralleling the scapula. Many books on many other breeds have made the same error; even some written by well-known judges who should have known better than to report on something they did not experience in real life.
From experience both in radiographing live, standing dogs and in feeling for the bones in the hindquarters, and getting my seminar attendees to do the same, I have repeatedly shown that the femur is vertical when the metatarsus (hock) is vertical. The natural stance for German Shepherd Dogs is with one rear leg placed a little (and only a little) under the torso for added support of a long, substantial body. In this leg, the femur is not vertical, but neither is the hock. Stand your dog with metatarsi vertical and parallel. Lift the dog’s rear leg while you feel with your fingers for the acetabular (hip) joint capsule, and make a chalk mark there. Then feel the depression between the upper and lower leg bones. This is some distance below the patella, which is too hidden in cartilage to be accurately palpated. Make another chalk mark there. You can now see that the femur is quite vertical between these two easily-located points.
The slant of the lower thigh in the GSD can roughly approximate that of both the croup and the humerus, although there is considerable variation, and it probably comes closest when the metatarsus is vertical, but even then not in all dogs – too much has been made of this similarity and the concept should be dropped. The angle that the lower thighbones make with the femur in a natural stance is not a right angle. Here again I am forced to contradict a poorly worded line in the AKC Standard which is more fancy than fact, and probably harks back to the days before radiography was used much.
Even von Stephanitz may have understated conditions a little when he said this angle should be “90 to 100 degrees, sometimes even a bit more.” He was talking about the angle made between the pelvis (croup) and femur, which right angle we have shown is not possible. But one of the axioms of geometry indicates that if the croup is parallel with the tibia, the angle between the femur and tibia equals that between the femur and croup. Remember that this premise of parallel lines is approximate at best. The angle between pelvis and femur is not a 90° angle, as you now know. With a slope of (typically) 35° to the croup, and a nearly vertical femur, that angle between lower thigh and femur in most excellent moderately- or even very-angulated dogs will be around 125° (90 + 35) from the horizontal, however one measures it. To have a right angle would necessitate a horizontal croup or a forward-slanting femur, neither of which are found. The angle between a vertical line from hip socket through the stifle indicating the femur, and the line from stifle joint to point of hock varies from 95° in an “extreme” dog to about 130° or 140° in a less-angulated, straighter-stifled dog. This means the angle of the lower thigh from the horizontal varies from 5 to 50 degrees in various breeds. The relative length of the lower thigh is the biggest anatomical factor in determining this angle. See Figure 6.
For a good understanding of the anatomy of the dog, additional pictures and discussion would be helpful. Toward that end, I urge you to get your own copy of “The Total German Shepherd Dog”, regardless of what breed you have, and study the illustrations and information.

Fig.1 Shoulder Angles – It is almost impossible to duplicate, by eye or hand, the typical illustration in most books that shows a 90-degree angle between limbs, with lines going through the middle of the humerus and from either the most-forward point of the shoulder or the imagined location of the center of articulation to the highest point of the scapula or along the scapular spine. Only in the “best” fore-assemblies will an angle of 90 degrees even be approached, and then only if lines are drawn on radiographs from top of ulna to front of upper arm to a point behind the highest point of the scapula.

Figure 3 Various Bone-Joint Angles in a Well-built Herding/Working Breed
(Actually, few GSDs have this good a shoulder, and very few from American lines since the 1970s)





Figure 6 Rear Angulation. This is defined as the angular relationships between croup (pelvis), femur, lower thigh, and metatarsus. The term is erroneously used by rank novices to describe slope of topline.
Copyright 2005 – This article is a revision of the earlier article “Angulation Front and Rear” by the same author. See separate article on hindquarter angulation elsewhere.
(About the author – Fred Lanting is an SV breed judge, is approved by UKC and many international registries as an all-breed judge, and has judged numerous countries’ GSD Sieger Shows and Landesgruppen events, and other shows in about 30 countries. He presents seminars and consults worldwide on such topics as Gait & Structure, HD and Other Orthopedic Disorders, Anatomy, Training Techniques, and The GSD. Fred lives part of the year in Alabama, actively trains in schutzhund, and breeds for occasional litters. He invites all to join his annual non-profit Sieger Show and sightseeing tour. He can be reached at mr.gsd@netscape.com and his dogs can also be seen on Jagenstadt, www.SiriusDog.com, and www.fredlanting.org; the latter being where you can also find most of his articles. Some of the illustrations in this article are from the book, The Total German Shepherd Dog. That book and the new Orthopedic Disorders book are available directly from the author or some distributors. Reprint permission of these copyrighted pieces can be requested and must carry this or a similar notice at the end.)
Predictions for 2008
Every year some of my GSD friends ask me to look into my crystal ball and predict the main winners of the upcoming Sieger Show. It might be fun to pretend that I’m clairvoyant, but my prognostications really are based on more mundane things: my background as an SV judge; I know the judges who are officiating; I go to the Sieger Show every year and visit top kennels most years; and I know the SV system. While there may be some surprises, such as dogs being sold to China and not being available for the show, I usually predict with about 85% or greater accuracy who will be in the VA males classification, and many who will be high-V.
While Quenn Löher Weg probably has many more winning offspring and will likely have the most impressive progeny class, it will be very difficult to beat last year’s Sieger Pakros. For one thing, Pakros has a Sieger as his sire and Quenn does not. For another, a German is one of Pakros’ owners, while Quenn is owned by a Brit. Now, Pakros is six years old and traditionally dogs of that age are retired, so it’s possible that Pakros and last year’s VA3 Dux (same age) may stay home this year. That would indicate that the battle would likely be between Quenn and the Pakros son Vegas du Haut Mansard. Vegas has also been used a lot for breeding, and will have a big progeny class. He has the advantage of having a Sieger for a sire and of being partly owned by Pakros’ German handler. Believe me, these nuances really do play a part in this “German national show”. His drawbacks include “near-normal” hips and a very wide action in front (seen coming toward you), which he passes on to most of his offspring.
I think Orbit Huhnegrab will retire or sit this one out, and the fight for VA3 will be between Nando Gollerweiher and Ingodds Agazzi; I predict the latter will pass Nando. For VA5, the very handsome Yak son Odin Holtkaemper Hof might move up. Godalis Tino will almost certainly be VA this year, but probably behind Uran Wilhelmswarte, so look for them around the VA6 – 9 spots. The other ones in that neighborhood could well be the Mack Aduct son Aron Terra dei Forti and the Zamp son Negus Holtkaemper See. Budiman Salihin’s Yerom will probably be in the V1 to V3 area, right next to Quantum Fiemereck (a wonderful dog with great pedigree). I doubt the Larus son V1 Yimmy Contra will be there this year.
Dogs to watch for, many of whom should be high in the V category: I hope Reinhardt gives a better placing to the exciting Timo son Arex vom Herbramer-Wald than he’s had the last couple years. This crowd favorite has the same marvelous shoulder opening and reach as his sire and carries on the qualities of the great Quando Arminius. The Peruvian Xaro v. b. Harten (Zamp Thermodos son), Digger Elzmündungsraum, Taureg Bad-Boll, Furbo degli Achei, Bruno Val D’Anzin, Tiras Roten Feld, Panjo Kirschental, Sony Heinrichplatz, Jumbo Zenevredo, and X-Box Precision. A dark-horse (surprise) high-V winner might be Arex v Haus Neoplantum.
Bitches are a lot harder to predict, because they often make one big splash in the competition, then go to the whelping box for the rest of their fame. But you should see the Negus daughter Paula Gut Lethe near the top; she really knocked my socks off last year. Other top prospects for Siegerin are Lana Zenteiche and Chanel degli Achei, with Anika Herdersfarm and Nadia della Loggia dei Mercanti close behind. Ronja Haus Burow will be high in the standings. If she shows up, Benny d’Ulmental also should be in the top group. Watch also for Tiana Fichtenschlag as well as Viana Fichtenschlag, Anika Herdersfarm, Romina Piste Trophe, Hazel vom Winnloh, Rimini vd Zenteiche, Birdy du Domaine du Parc, Palme vd Zomerdijkslanden, Biene vom Valtenberg, Flora di Casa Nobili, and Pitty vd Freiheit Westerholt,
Things that can throw my predictions off include sales to people in foreign countries, bitches talking time off for whelping or blowing their coats for estrus, and of course a poor performance in the courage test. So many show dogs are given “passing grades” at the Friday courage test, that they are seen by the breed judge later without any indication that their character was not really what is worthy of high placings. That is why I want to see as many of these dogs doing their bitework as possible, and make up my own mind as to whether they deserve the breeding recommendations that come with a high Sieger Show placing. Friday is a long day, but unless you tough it out and see what the dogs really have in them, you can be fooled by how they do the next day.
Tell your GSD friends to join my group next year. If you, the reader of this little forecast, are going on this year’s tour, compare my predictions, stay close in case you have questions, and enjoy!
Fred
Fred Lanting, annual Sieger Show tour director.
A Small Problem: Dwarfism in Dogs – Part 3
Confusion Continues
Fred Lanting
This is a follow-up article to the one I wrote entitled “Osteochondrodysplasias” in February of 2004. While that was a rather long piece, it still did not address all that people want to know about the subject. Nor will this, but at least we can look at some other aspects, including a little deeper delving into the questions about the genetics of dwarfism.
There are miniature and toy versions of “standard”-size breeds, but this is not the same as dwarfism, the latter being the result of an abnormality rather than a variation within normal limits in genes. People are always developing miniaturized strains by selectively breeding small examples to each other, and continuing to select until “regular” size individuals no longer appear. Some years ago, the heiress to a margarine fortune started to develop miniature Borzois. While some detractors accused her of using Whippets to jump-start the reduction in size, it really doesn’t matter much. Livestock breeders know that you can introduce a gene for some dominant characteristic such as color, but then keep breeding the other structural phenotypes back into in the original breed in such a way that the “new breed” (really a minor variation on the one they started with) will look and perform no differently, except for that color. Or whatever trait they want to introduce.
There is also no reason to believe she did not simply choose the smallest Borzoi from her extensive kennel and, in successive generations, bring down the size until the partners would “breed true”, in regard to that characteristic while not losing proportions or other qualities. Several years earlier, another woman developed a strain of Boxers that matured at 12 pounds body weight by selective, not cross-, breeding. While these examples never caught on, numerous such projects have, to some extent: the Shar-Pei, Australian Shepherd, Teacup Poodle, Bull Terrier, and numerous others. Miniatures do not have enough genetic change to classify their genes or body phenotypes as “abnormal” and, with the minor exception of a little difference in the head, miniatures have the same proportions.
There is a type of dwarfism that also produces proportional but suddenly smaller dogs. I say “suddenly” because unlike the “breeding down” through many generations, proportional dwarfs appear without successively smaller individuals in the line of descent. So far, I have found the particular type that I am thinking of, in only the German Shepherd Dog and in a breed with the GSD in its ancestry, the Karelian Bear Dog. Affected dogs are called Pituitary Dwarfs because the immediate cause, or at least the noticeable defect, appears in the hypophysis on the bottom of the brain. The anterior lobe of this endocrine organ is rightly called the “master gland” because of its governing or influential effect on other organs, specifically the glands. Minor abnormalities in this gland are what create the body types of Bulldogs, the acromegalic Saint Bernard, Dachshunds, and endless other examples of a departure from the more “normal” or “ancestral” types such as the GSD, sighthound, Pointer, etc. Anatomic and functional abnormalities in different parts of the hypophysis make for the difference between the Boston Terrier and other breeds intentionally selected for their abnormalities, for example.
Proportional dwarfism in the GSD is called “pituitary dwarfism” because an old name for the hypophysis, or part of it, is “pituitary gland”. Since this master gland controls much of the activity of other glands, it is not surprising to see abnormalities in thyroid function, and thus the inability to grow a normal coat. Most pituitary dwarfs look like Chinese Crested or other “hairless” breeds although by carefully dosing with thyroid hormones (and possibly the more expensive growth hormones), a normal coat can be maintained. See my article in the December 1984 issue of Dog World, which I may re-issue if there is enough interest. We can deduce that it is caused by a defect in a different part of the pars distalis of the hypophysis than different types of defects or in different gland parts in other breeds. We can make such deductions because such breed differences have been traced to such anatomic irregularities by Stockard and others at least as far back as the 1940s.
The non-proportional canine dwarfs, like their human counterparts, result from genetic defects that take root in other parts of this master gland, and therefore other endocrine glands and organs. But there is much confusion, disagreement, and lack of knowledge leading to frequently inadequate definitions. In my other article, which you might call Part One of a trilogy, I mentioned that various terms are used; I would like to here suggest that we settle on one umbrella word to cover all or most others: either chondrodysplasia or chondrodystrophy. The first simply means an abnormal development or shape (-plasia) of cartilage (chondr-). The latter is “translated” as poor (dys-) growth (troph-) of cartilage. Either would be a less cumbersome term than I used as the title of Part Two, osteochondrodysplasias, which includes the “osteo-” simply to emphasize that the bones are also abnormal. I think we do not need such a mouthful, and that readers will assume the inclusion of shortened bones in the term “chondrodystrophy”. A possible drawback to using chondrodysplasia is that it might someday be confused with enchondromatosis, a rare disease often involving tumors; these words are used interchangeably in human medicine. On the other hand, chondrodystrophy is sometimes used as part of a longer term for different disorders, also. Most of the time, though, it refers to a congenital defect in the formation of bone from cartilage.
Achondroplasia is one of those words that uses the prefix “a-” to denote or connote an absence or deficiency of something. In this case, it means a lack of (good) shape, growth, or form of the cartilage. Aplasia, for example, means “lack of development”, as illustrated in my 2004 book by the radiographic picture of an Airedale whose acetabulum and top portion of the femur did not develop at all from cartilage. The achondroplastic limbs of the Dachshund means that these extremities failed to elongate like the development in normal dogs. Achondroplasia of the skull is obvious in the Bulldog. In either example, the word refers to a disordered chondrification (and of course, later ossification) of the ends of bones. In most breeds, this is most obvious in the long bones (limbs). It is simply arbitrary preference that I use the words chondrodystrophy and chondrodysplasia more often.
But what about the genetics? To even attempt to delve into the mysteries of inheritance of various forms of dwarfism, one must be prepared to consider different genetic causes and expressions in what, on first glance, is easy to assume are the same conditions. Only by crossbreeding can we make better guesses. A couple of the most active researchers into inheritance of traits and practitioners of crossing breeds to get answers were Stockard in the 1920s to `40s, and Whitney in the `30s to `50s.
Basset breeders know that achondroplasia is dominant in their breed, and some think that this means the F1 progeny will always have the same leg length as the Basset. But in crosses between Bassets and GSDs, typically about half the legs (dogs) are intermediate in length, the other half being normal (long, GSD-type) in length. The same when a Bassett-Bloodhound with intermediate-length legs is crossed to a long-legged dog such as the GSD or any other breed.
Cocker Spaniels often have shorter-legged individuals, but the mutation to achondroplasia is not frequent, and is definitely recessive. Other races breed true every time, such as Corgis. It appears that “reverse mutation”, that is, a normal-leg-length offspring being produced by two typical Corgis, just does not happen. Yet we know that we can suddenly find Corgi-style legs in purebred pups of Cocker, German Shepherd, and other breeds. Corgis (and dogs with this mutation suddenly appearing) may have a slightly different genetic code and type of dwarfism than do Bassets and Dachshunds. English Bulldogs seem to have a type of dwarfism more like the Basset than the Corgi. The short legs of the Clumber Spaniel or the Beagle are almost certainly not examples of true dwarfism, as the shapes of the joints and bones are more like those of the normal-length breeds. Sometimes non-dwarf short legs are selected for by misguided breeders (and the judges who reward their dogs!), as in the cases of modern Golden Retrievers, and GSDs from American or “Alsatian-British” lines. There is still a great deal to be sorted out, when it comes to defining the genetic differences in the dwarf dogs. Only when breeders are open and honest, and share their experience and dogs with researchers, will we make progress in unraveling the rest of this riddle.
© All use of the above must be by prior permission, and carry this copyright notice. Fred Lanting, Canine Consulting. Seminars: Canine HD & Other Orthopedic Disorders; Gait & Structure (Analytical Approach); more. Fred is an international all-breed judge, and senior lecturer in anatomy and can be contacted at: mr.gsd@netscape.com
Articles can be found on many additional websites.
Osteochondrodysplasias, Leg Deformities, and Dwarfism in the Canine
Osteochondrodysplasias, Leg Deformities, and Dwarfism in the Canine
(Part 2 of a series on dwarfism)
© 2004, Fred Lanting
There has been renewed interest in the subject of “abnormal” bone lengths, joints, angles between limbs, and related phenotypic variations from what I have called “the ancestral type”. We need to establish some definitions of terms before entering into a discussion of the subject. The “ancestral” phenotype in my arbitrary definition (which, however, is in line with the views of many or most professionals in animal science) is one that comes to mind when one thinks of the Jackal, Northern Wolf, and descendants of the extinct Pale-footed Wolf (such as sighthounds). The head is neither brachycephalic (pushed-in/shortened) nor exaggeratedly long and narrow (the dolichocephalic Borzoi, etc.), the leg length is such that the total height at withers is roughly twice the distance from elbow or chest to the ground, and limbs give an impression of being straight. Typical examples of ancestral types are the German Shepherd Dog, Saluki, various Spitz breeds, and many pariah breeds such as found in every corner of the world.
“Abnormal” phenotypes (and this will rouse the ire of many people who love their dogs and think of them as being “normal”) include breeds specifically bred to produce the characteristics that would be agreed on as being “faults” in the ancestral types. Think of the (“English”) Bulldog, Pekingese, Corgis, Dachshunds/Teckels, and others. I have long maintained that there is a genetic defect affecting primarily the hypophysis or pituitary gland, the “master gland” that so greatly influences the functions of the others as well as developmental processes.
Some variation within normal parameters results from the tremendous plasticity of the canine genotype, but here we are more interested in the departure from those limits of normality. Whatever the combinations of defective DNA nucleotide pairs (adenine-thymine, cytosine-guanine, etc.), and which glands or organs they initiate the changes in, many of the irregularities we are discussing here manifest themselves in the cartilage that is on the ends of bones and “bone centers”. Bone centers are those hard, mineralized portions of a growing bone that become enlarged (almost entirely on their long-axis surfaces) and fused together to form the eventual limb, and the cartilage between most bone centers is called a “growth plate” or physis. It gradually “calcifies” into bone tissue, thus uniting epiphysis (called a cap or head, usually) and metaphysis (shaft); it disappears during maturation. But if there is an abnormal coding of the nucleotide pairs, there is an abnormal calcification process, a “growth-plate disturbance”.
If one bone in a two-bone limb segment (such as the tibia/fibula or ulna/radius combinations) has more of a disturbance than the other, or if one end of the growing bone’s cartilage is disrupted during remodeling into bone tissue, there are unequal rates of growth and consequent bowing of that limb, with one part wanting to be longer than the other part does. In some dogs, disruption of normal cartilage-bone turnover at the ends can keep a single bone from growing in length, or if the disruption is laterally asymmetrical, the femur or humerus may also become slightly bowed. The pull of muscles and ligaments on different parts of such bones also has some effect on shape.
The general definition of “dysplasia” is poor or abnormal (dys-) shape or form (-plasia). Here, we are talking mostly about bone (osteo-) and cartilage (chondro-), and mostly about those tissues in joints. But just as the poet says, “no man is an island”, and genes that cause one thing can sometimes also cause something else. Some times it is a very obvious double influence, such as the gene that causes both deafness and white coat phenotypes in some breeds, or dwarfism and blood disorder in the Malamute. Most of the time, the influence of one gene or set of nucleotides is less obvious.
A couple more definitions would be helpful at this point, although you should realize that there are sometimes loose adherence to strict interpretation of such definitions:
chondrodysplasia: any growth plate (cartilage) disturbance resulting in canine dwarfism; in human pathology, it has a different meaning: enchondromatosis, a rare disorder marked by enlarged cartilage and tumors in joints.
chondrodystrophic: semantically similar to the above, but while –plasia refers to changeable shape, –trophic refers to growth. Thus, an abnormal cartilage growth pattern.
achondroplasia: that type which results in an individual with extremities shorter than the trunk. Examples in dogs include Basset Hound, Shih-Tsu, and others mentioned elsewhere. In humans, it usually is marked by stubby hands, large head with sunken nasal bridge and, frequently, spinal column deformities.
CHONDRODYSTROPHY
Several breeds are of a body type we call chondrodystrophic, such as the Dachshund and Corgi. They have shorter legs (often bowed) and other dwarf characteristics in parts of the body. Frequently, these breeds also have a shorter vertebral arch that tends to produce a smaller vertebral canal. The vertebral body centers of ossification unite with the arch prematurely, with the same type of dystrophic bone growth pattern that causes shorter “long bones” in those breeds. See Chapter 16 in my 2004 orthopedics book for more illustrations and discussion on dwarfism. In some chondrodystrophoid breeds such as the Basset, a premature closure of the distal metaphyseal plate of the ulna (near the wrist) was thought by Herron, Grüll, Henschel, and von Hitz to cause fracture of an already closed anconeal process at the other end of that limb. Kasström and colleagues (and later, Wind) thought that this condition in certain dwarfed breeds “was the result of an abnormal pressure on the anconeal process… by the shortened ulna.” This anomaly in the anconeal process is not the same as the failure to unite, and obviously has a different genetic origin. Dr. Wind, the eminent expert on elbows, has observed that many cases of elbow dysplasias include subluxations associated with dwarfism
There are many types of dwarfing related to slow endochondral bone formation (at the ends). Dwarfism can be proportionate or disproportionate, depending on the specific gene defects. Examples of the former include the pathological pituitary dwarfism of the German Shepherd Dog and the related Karelian Bear Dog. You can see GSD pituitary dwarfism in “The Total German Shepherd Dog” (www.Hoflin.com). The non-pathologic selective miniaturization seen in Shar-Pei, Bull Terriers, Australian Shepherds, Poodles, and numerous other miniature and toy breeds and varieties probably should not be included in a discussion of dwarfism. Disproportionate dwarfs include Bulldogs, Basset Hounds, Pekingese, Dachshunds, Corgis, and many more that we see only in this form. While some would object to inclusion of their favorite breed here, it is still true that these are results of genetic defects. There are also “unnatural” occurrences of disproportionate dwarfism in breeds where you might not expect it: Malamutes, GSDs, and a few other “accidentals”. Of course, if one were to deliberately linebreed on these defects, a sub-population of short-legged representatives would be more common. That is what happened with a branch of the Parson Jack Russell Terrier, now known by several similar names in various show registries.
Some of these defects involve irregularities in the construction of the hypophysis (pituitary gland), as I have said; others may involve primary proteoglycans degradation that results in mucopolysaccharidoses, or other metabolic abnormalities. The various types of mucopolysaccharidoses involve enzyme deficiencies, incomplete fusion of the sacrum, incompletely developed vertebral end plates, short limbs, abnormal joint mobility, and other signs and deformities. Some osteochondrodysplasias (you now know how to break that word into segments, and what they mean) can be recognized at birth, others not until skeletal maturity approaches. The most common seen at birth is the achondroplasias of rabbits, mice, and humans, although some (erroneously?) apply that term to conditions in dogs, too. Some achondroplasia is from sporadic mutation, and most seem to be transmitted by a dominant gene. A few authorities have claimed that achondroplasia is not seen in the canine, but Aegerter and Kirkpatrick describe it as a genetic chondroblast (cartilage cell) disturbance in the epiphysis. Betts calls it “a symptom rather than a disease” and does not hesitate to apply the word to the “normal” condition seen in the Dachshund, Beagle, Basset Hound, French Bulldog, Pekingese, and similar breeds. He properly excludes pituitary dwarfs, miniaturized but proportionate breeds, Malamute dwarfism, and the dwarfism of Labs with retinal dysplasia. Various forms of chondrodysplasia affect Cocker Spaniels and German Shorthaired Pointers.
Miniature Poodles are occasionally found with a form of osteochondrodysplasia that has sometimes but properly erroneously referred to as “achondrodysplasia”. An increased collagen concentration and RNA content is often found in affected cartilage of such dwarfs, though DNA content is normal. There are differences in appearance between individuals because of modifier genes as well as environmental forces. Miniature Poodles with inherited epiphyseal chondrodysplasia are rhizomelic (it seems the shortness of their limbs comes primarily from the retardation of growth nearest the hips and shoulders) and often have ventrodorsal compression of the chest and enlarged joints. Occasionally a spontaneous mutation will produce symptoms similar to congenital spondyloepiphyseal dysplasia and “achondrodysplasia”, and variations on these are seen in many breeds, including multiple epiphyseal dysplasia in Miniature Poodles and Beagles.
Asynchronous (unequal) growth of the radius and ulna, that is, when these two bones’ growth rates are not coordinated, is found in non-dwarfs in a wide continuous “spectrum” of severity, often unnoticed by the average dog observer (and many a licensed dog-show judge!). Dwarfism is often an accompaniment to that asynchronous growth of the “double bones” in either front or rear limbs. Such dogs also have nearby limb segments shortened, such as the humerus or femur. The more extreme end of that range is considered by some to be “normal” in some breeds (to name some more: Corgis, Basset, Lhasa Apso, and Pekingese). However, elbow subluxation accompanied by pain has been reported in these dwarf breeds, and probably has a causal connection. While carpal valgus (turning out at the pasterns) and external rotation of the foot are “acceptable” within the descriptions of “breed type”, the occasional or perhaps frequent abnormalities of the ligaments and joints in the elbow that accompany this should be avoided or treated.
OTHER SIGNS
Chondrodysplasia in the most general sense is sometimes called a syndrome, other times part of a syndrome, the definition of that word being a collection of interconnected symptoms. Some dogs may have many, some a few, and others no readily observable symptoms. The clinical signs may be very mild, from almost undetectable bowing or shortening of the legs, to obvious skeletal deformity and the presence of several health problems. Chondrodysplasia Punctata is one name applied to a syndrome of multi-systemic disorders, and is so-called because of the “dots” of calcium phosphate deposits in the softer cartilage. It reminds me of the school of art made popular by Georges Seurat called “Pointillism”. This genetic-metabolic problem has various skeletal expressions. Depending on the particular variety, the mode of inheritance could be autosomal recessive or dominant, or X-chromosome-linked recessive or dominant, some with full penetrance, and some not.
Besides skeletal indications, there are eye disorders such as microphthalmia (smaller eyes than they should be), lens detachments, cataracts, glaucoma, retinal defects, and nystagmus (jerking or twitching of the eyeballs). Other occasionally reported symptoms are problems with internal organs, head and neck bone defects, partial deafness, alopecia, and luxated patellas (for more on this stifle problem, see my upcoming orthopedics book or some of the websites that carry my articles).
PREMATURE PHYSIS CLOSURE
Premature closure of growth plates happens because, in some etiology (manner), the ossification process of endochondral cartilage is disturbed. Overfeeding and mineral supplementation are definitely contributors, but genetic susceptibility has to be taken into account, as well — probably much more. Ettinger mentions that “the most common cause of premature growth interference has been direct trauma to the growth plate area”, though HOD and achondroplasia have also been reported in association with it. But he and his sources may have been giving too much credit/blame to physical or mechanical damage. The distal (furthest part) radius and ulna seem to be the most frequently involved sites for these disturbances.
Growth disturbances in the radius and ulna can be related to an outward twisting of the top of the ulna away from a good fit with the humeral condyles, enough so that subluxation or even luxation takes place. This lateral rotation may also exist independently, with no observed growth plate disruptions in those bones. The radius head can also dislocate, and both may occur at the same time, so there is quite a variety of changes possible, although the disorder is rare.
If the dislocations are not accompanied by (or secondary to) such asynchronous growth manifestations as seen in the ulna and/or radius, they are called congenital elbow dislocations. The premature closure of physes in ulna or radius, retained cartilage, chondrodysplasia or achondrodysplasia, and synostosis are separate problems. A condition of missing digits called ectrodactyly and another abnormality called cleft hand deformity have been seen in conjunction with congenital luxations and subluxations (also called arthrodysplasia) in the elbow.
ROOTS OF MANY OF THESE DEFECTS
Cholesterol has had a bad name among fad-diet promoters and people too lazy or busy to physically work off their calories. It is a product of the liver, necessary for the synthesis of Vitamin D as well as the assimilation of it, essential fatty acids, and Vitamins A, E, and K, but in sedentary people and those with genetic inability to metabolize it correctly, it can build up in the blood vessels and contribute to heart disease and stroke risk. At least some chondrodysplasias involve an error in the coding for biosynthesis of cholesterol. Since in the Havanese, a miniature Cuban breed, those who evidenced this dwarfism tested as having abnormal levels of several cholesterol-related sterols, a program of blood serum testing was undertaken. It was found that Havanese with normal straight legs had no such metabolic abnormality. in the body. These vitamins are needed for calcium utilization, bone development, and healthy eyes. The appearance of congenital defects, including osteochondrodysplasias, can often be blamed on inability to use these chemicals. Tracing a structural defect to its headwaters of a genetic defect expressed in a metabolic disorder along the route, is akin to finding the source of the Nile or Amazon.
PLEIOTROPIC DEFECTS
Pleiotropy is the phenomenon of having more than one phenotypic expression (often in grossly different manifestations) caused by the same gene — the same genetic defect. Alaskan Malamutes’ dwarfism is a pleiotropic genetic defect that shows up as both dwarfism of their particular type and a blood disorder. It has been fairly extensively studied, and while one dog may vary in appearance considerably from the other, the disorder is a simple autosomal (not sex-linked) recessive trait with complete penetrance. Asynchronous growth of the radius and ulna (one at a different rate or completion than the other, remember) is part of the deformity in this breed. The chondrodysplasia in this breed has at times been mistaken for the Vitamin D deficiency called rickets, but only the tubular bones are affected, other than retarded ossification of the lateral tarsal (cuboid) bone. The head, spine, and other bones are not stunted or changed, and body length is normal. The gene that causes this chondrodysplasia also creates a macrocytic hypochromic anemia; the discovery of this being indicative of the way carriers may be found. A third effect of this one gene, by the way, is a different ability to bind certain trace minerals in the liver.
While on a judging assignment in Alaska in the early 1980s, I was presented with a Malamute from show lines, which had from an early age walked flat on its wrists. Because the forearm did not appear bowed I initially thought it might have been a case of carpal luxation syndrome that I had been seeing with increasing frequency in American German Shepherd Dogs. I lost track of the owner and did not see any radiographs or blood analysis. Later, after seeing more Malamute Chondrodysplasia, I reconsidered my tentative “diagnosis”. I think now that it could possibly have been both disorders occurring concurrently in the same dog, but more likely the carpal luxation was a result of the chondrodysplasia gene. Unfortunately my photographs of that dog were lost, but I later obtained pictures of other Malamutes, though without the extreme flat carpus.
A few other problems are similar, in that one gene (or gene pair, really) can cause ocular-skeletal dysplasia in Labrador Retrievers and possibly Samoyeds, for example. In this disorder, several defects in the eyeball, iris, and arteries serving the eyes are found in the same dogs that have short, thick leg bones (micromelia), prominent carpi (wrists) and elbows, and east-west stance in front. Hind legs usually are hyperextended (straight in stifle) yet still very short.
Great Pyrenees have their own style of micromelic dwarfism, too, as do a few other breeds. It is a simple recessive genetic trait, showing some similarities to Malamute dwarfism, and is marked by short curved ribs, underdeveloped rear limbs, all legs shortened, and abnormalities in the cartilage and bone of the vertebrae. Endochondral ossification disturbance can usually be seen on radiographs by 8 weeks. Often, ossification of the vertebral bodies, especially in the neck, is delayed right from the beginning, and visible on radiographs taken at 8 weeks of age. The metaphyses of the radius, ulna, and tibia are usually flared like the bell-bottom trousers of the hippies in the early 1970s or the sailors of a generation earlier. The condition does not automatically result in DJD (degenerative joint disease).
Norwegian Elkhound chondrodysplasia is similar to the other canine dwarfisms as well as to human spondylometaphyseal dysplasia; it is widespread in the breed, and may be associated with glycosuria (sugar in the blood), although in one study this was not found. Some curvature of the front legs may be noticed as early as 5 weeks of age, and all limbs are short in proportion to the body. It is also a simple recessive trait.
A disorder almost identical to the chondrodysplasia in two of the above-named breeds has recently been found in Akitas. Knowing how such reports usually lead to the identification of the same disease in other breeds (as has happened in panosteitis, GSD myelopathy, etc.), it is not very risky to predict that more will be added to this list in the future, though not at a high rate, given the very obvious nature of dwarfism and most breeders’ desires to sweep it under the rug or eliminate it.
On an excellent website calledhttp://www.rhosyngsd.com/, there was a good description and illustrations of dwarfism in the Havanese breed, and an ancillary discussion of dwarfism in the GSD, even though the site owner did not want to use that word for the condition. Havanese with dwarfism display ocular abnormalities as do a few other breeds. The front legs grow crooked or bowed, and all four legs are shortened, giving the height-to-length ratio an undesirably short aspect. Some Havanese breeders have reported that all cases of early-onset cataracts leading to premature blindness, and nearly all “other serious health problems reported in Havanese within the past few years, have been in dogs that also exhibit the symptoms [of chondrodysplasia]”. In Havanese, it also has been noted that some dogs have such subtle signs — that they appear to have a straight leg on one side but not the other — asymmetric. Furthermore, one breeder asserts, such asymmetrical dogs, if they are also diagnosed as having cataracts, will have the cataract in the eye that is on the same side as the crooked leg! The Rhosyn website mentioned says, “To date, no Havanese with straight legs have been diagnosed with early onset cataracts!” It must be added, however, that other long-time Havanese breeders deny any connection. It could well be merely coincidence. In fact, unless pleiotropy can be established, it would be best not to put much stock in the Rhosyn observation.
Many other dysplasias considered as a subcategory under osteochondrodysplasias result from disturbed ossification along the periphery (outer edge) of the growth plates in various bones such as the ribs, vertebral processes, skull, and elsewhere. Certain dwarfism characteristics have been made part of the breeds’ show standards and are not much covered here, but even some breeds that are not normal skeletally, anyway, such as Dachshunds and French Bulldogs, sometimes are even more afflicted with chondrodysplasia than their artificially-considered “normal” compatriots. In many cases, dwarfisms with partial penetrance or expression may go unrecognized, with the breeder considering the mildly affected pup to be simply a “runt”.
Recently, some cases of chondrodysplasia/chondrodystrophy of the sort found in the Corgi have been reported in German Shepherd Dogs in Australia. The German Shepherd Dog Council of Australia website, http://www.gsdcouncilaustralia.org.au , has some more details on the investigation there. Some of the bitches whelping such dwarfs are daughters of popular showdogs such as Hammer v Waterkant, Lindendale Strike Force, Leitungen Prince Rowdy, and the highly-respected German export Iwan v Lechtal. Cases have been reported all across the country: in Canberra, South Australia, New South Wales and Western Australia. One cryptic comment from Downunder was, “The common denominator in all cases has been the Stud Dog.” I found this dog is Aimsway Abacus, a son of German import Balou v Eppelin and a local-bred bitch, Rakishka Ali; Abacus linebreeding is: Eiko-Vasall Kirschental (5-5). Most people are reluctant to `fess up to genetic problems for fear of losing face — or stud fees. Fortunately, there is a move for openness in Australia concerning this appearance of achondroplastic dwarf GSDs, even though at this time it appears the incidence is considerably less than the incidence of pituitary (proportionate) dwarfism in the GSD that I reported on several years ago. Some examples of the latter are shown in my GSD book.
Pituitary Dwarfism in the German Shepherd Dog (Part 1)
Part of a Set of Articles on Dwarfism
by Fred Lanting
(original version appeared in Dog World [US], Dec. 1984)
Dwarfism is a condition of abnormally small stature, and usually is characterized by altered body proportions. Dachshunds, Basset Hounds, and Corgis are examples of achondroplastic dwarfs; they have more or less normal-sized torsos and heads but shortened limbs, and are accepted as typical of their breed. Alaskan Malamutes, on the other hand, are not considered acceptable if they have their particular blood cell related disease. In that breed, both achondroplastic dwarfism and hemolytic anemia are inherited as pleiotropic conditions, meaning a single gene giving multiple phenotype effects. Additionally, there are dwarfism abnormalities in other breeds such as pseudochondroplastic dysplasia in Miniature Poodles.
In the German Shepherd Dog, however, there is a little-known dwarfism that yields a nearly perfectly proportioned but considerably downsized version. An acceptable term to use would be proportional or pituitary dwarfs, even though all types of dwarfism have their origins in that gland. The fact is (or was until this article appeared), many do not know about the existence of this type of dog, even though it is not all that rare. Possibly because of the large-scale linebreeding by a West Coast kennel that produced winning dogs, the incidence rose for a number of years in the U.S. Due to linebreeding on certain British and German dogs, there was a noticeable number appearing both in England and Australia, countries which rely heavily on German lines. One genetic analysis of Australian data indicated that two dwarfs might be expected out of 1000 pups when “any dog” is bred to “any bitch”. The recurrent risk for any dog or bitch bred to a parent of a dwarf is seven per 1000; a parent of a dwarf to a half-sibling of a dwarf is 272 per 1000; and parent of dwarf X parent of dwarf is 235 per 1000. The roughly 25% risk in the latter two matings is typical of what one would expect when two normal carriers of a simple Mendelian trait are bred to each other.
Of course, that 25% is an average. I recently (1984) examined pups from a litter of six in which three were pituitary dwarfs, but both parents were of normal size. Now remember, these were not abnormal in proportions, only in size and unseen body chemistry. The little Shepherds I examined that year had beautiful temperaments, and were active and apparently healthy at the time I first saw them at almost four months of age. They weighed about five pounds, while a normal littermate was about 32 pounds. There was something that had not appeared in the scientific literature but which I noticed in this litter, as well as in photographs of other litters: pituitary dwarfs seem to squint in bright sunlight more than do their normal siblings. Another facial characteristic of miniature Shepherds is a fox-like appearance, coming from wide-set ears. I believe this to be a result of disrupted proportions of skull vs. base of the pinna (ear shell), which to some extent is seen in Welsh Corgis also. A somewhat snipey (pointed) muzzle is due partly to a shortening of the skull and, in some individuals, a slight overbite.
The Arkansas litter I visited was no combination of junkyard genes, but sired by an AKC Champion and with two Champion grandsires. The whole pedigree was full of recognized and respected kennel names and individuals. Indeed, the trait has been known for many years to be carried by “champion-quality” dogs. The gene seems to have first arisen, possibly as a mutation, around 1940 or shortly before. It’s almost 100% sure that one of the most valuable German Shepherd Dogs of all time, Vello zu den Sieben Faulen, is a major source in bloodlines since the late 1950s. But we cannot lay all the blame at his feet, nor avoid all his descendants. Nor would we want to, for many of the breed’s best lines are based on Vello. Only a percentage of his (or any dog’s) progeny would carry the defective gene, and presumably many of the earlier dogs who exhibited it in their progeny were removed from the gene pool. The SV doesn’t favor continued breeding of dogs that produce defects, and they have the power in Germany to prevent such dogs from further use by denying registration. However, when a dog is valuable in other respects, such as the Sieger Uran WildsteigerLand, a blind eye is used to look in that direction.
Some non-show lines occasionally come up with pituitary dwarfs, such as the white German Shepherd bitch I found, who at two years of age weighed only 15 pounds (some get as heavy as 30 pounds or so, but most are smaller). Her skin was milk-chocolate in color, thin, wrinkled, dry, and lacking in elasticity or tone. She had almost no hair on the trunk, neck, and wear areas such as buttocks, etc. Primary or guard hairs were present on a few areas of the head and feet, and the rest of the body was either bald or lightly covered with secondary hairs (puppy fuzz or undercoat), which were easily pulled out with the fingers. All these signs are very common in these animals as adults, with the skin ranging from brown to gray in color. Dogs which would otherwise be plush or long-coats usually look like Chinese Crested Dogs — if they live to maturity — with feathery fringes around the ears and feet, and bald elsewhere unless treated with growth and/or thyroid hormones.
External or obvious characteristics aren’t the only things different about pituitary dwarfs. Blood chemistry tests show that hormones that are supposed to be circulating may be absent or at very low levels. The methods are too involved to go into here, but briefly stated, there are ways to assay the activity of endocrine glands and amounts of their secretions. The hypophysis (commonly known as pituitary gland) is the “master” gland of the body, situated in the center of the head at the base of the brain. It produces a number of hormones, including GH (growth hormone). IFG (insulin-like growth factor) circulating in the blood is interdependent with GH. The pituitary gland is affected by others, but it is more the director of the body’s other endocrine glands, such as the thyroids and gonads. The thyroids have a say in the maturing process, metabolism, development of form and behavior, and physical and mental activity. Muscular weakness and the skin/hair problems described above are due to inadequate or absent thyroid activity, which in turn is due to lack of proper direction from the pituitary. Your veterinarian can explain T3 and T4 to you if you wish to study thyroid function more fully.
The effects of this type of dwarfism can be mitigated or delayed by administration of thyroxine and GH, but this is a very expensive proposition at present. It is thought that if recombinant genetics (gene-splicing) and RNA production of human growth hormone becomes feasible, the price may go down. Dogs apparently respond to human GH, but not the other way around. Eventually, at the age of normal skeletal maturity or a bit later, the growth plates in the dwarf’s bones close and no further growth is possible, regardless of GH injections. Another problem in treating the condition is that most owners don’t present the pups to a veterinarian until their littermates are twice their size. The affected pup grows normally until three to eight weeks, when the brakes are applied and the normal siblings leave him behind in growth.
Although it is possible that pituitary dwarfism in the GSD is a polygenic disorder of a threshold nature, most investigators so far believe it a result of a simple autosomal (not sex-linked) recessive trait. In most characteristics inherited in this simple method, the recessive gene can be hidden for many generations before it is paired with another identical recessive gene. Genes operate in pairs, and only when both of the pair are the recessive alleles, does the trait manifest itself. When only one recessive gene exists, its dominant partner dictates the normal or dominant phenotype characteristic. It’s like a Labrador Retriever that inherits one gene for black coat color and gets the recessive gene for yellow from his other parent. He himself is black, because that first gene is dominant over yellow and does not allow the yellow to predominate or show in the phenotype (appearance).
However, some recessive traits are only partially covered up by the dominant member of such a heterogenous gene pair. Often, one can see the faint hint of a saddle in a sable German Shepherd Dog which is heterogenous (has one sable gene and one black-and-tan gene). Similarly, it may be possible to “see” other recessives through the use of blood tests, examination of the eyes retina, etc. Achondroplastic dwarfism in the Malamute, for example, is connected with a blood cell disorder, both being pleiotropic results of the same defective gene. Because of the effect the pituitary has on thyroid function and on other glands, it may become possible to detect the “carriers” in a GSD litter among whose members some dwarfs have appeared. In a statistically typical litter of 12 produced by two normal-appearing carriers of the recessive gene, suppose three homozygous dwarfs and three pups without the gene. The other six are heterozygous carriers and appear normal (like their parents) but will contribute one recessive gene to each pup they produce in the future.
It is unfortunate that such abnormalities are often hidden from the public by breeders and owners who are fearful, mercenary, proud, or ignorant. Most pups are sold about the time the growth rate difference begins, so many cases reported to veterinarians have been “single incidences” as far as the buyers and their vets could tell. Others may be put down by embarrassed breeders who don’t want it known they have produced such anomalies. Since the health of pituitary dwarfs is more precarious than that of normal pups, it can be assumed that many that die at birth, are resorbed during gestation, or die before the trait begins to appear, may be dwarfs. The Arkansas breeder who called me to ask what she had, and invited me to see them, upon discovering half her litter were dwarfs, decided not to put them down and cover up, but rather care for them and share their stories with responsible breeders and veterinary researchers. She even intended to train and show at least one in obedience and was, at this first writing, hoping to persuade the AKC that there are no rules against it. From such an openminded approach, we may be able to make an educated guess as to pedigree origin of the defect, plus discover some means of identifying normal-appearing carriers.
She even briefly entertained hopes to try breeding these dwarfs with each other or with siblings or parents, trying to duplicate the occurrence. I guessed (correctly) that she might find it difficult. Development of the gonads varies from atrophied testicles and absence of estrus to normal testicles and seasons. If she had been successful in reproducing the condition, we may have seen the AKC faced with difficult decisions: they cannot justify withholding registration privileges or show/trial eligibility because of the pure pedigree, so do they create a separate variety within the breed, as exists in Dachshunds, or a separate breed as they did with Norwich and Norfolk Terriers? Doubtful. The only alternative is to keep them in the regular classification and hope judges will not place them for reasons of not being of sufficient breed type. The German club has disqualifications for those outside size limits; the AKC does not. By the way, for several years, a pituitary dwarf attended the German Sieger Show (as a spectator) and was seen by thousands.
One problem I can foresee in attempts at breeding these, besides lowered fertility, is whelping. Pituitary dwarfs start life off at normal size, which for a Shepherd is in the neighborhood of one pound, give or take about four or five ounces depending on the number of whelps. If a dwarf bitch were impregnated (artifically, of course) by a normal-sized carrier male, some of the whelps could be normal sized and the bitch would not be able to pass them or possibly even carry them without damage to them and/or herself. If a normal-sized carrier bitch were bred to a dwarf male, it shouldn’t be any more of a problem than when two normal-sized dogs with the recessives are mated together. So far, nobody has engineered such a mating, to my knowledge.
Size of the dwarfs varies a great deal. As of this (1984) writing, the ones I have examined were 5.5 months old and weighed seven pounds. Others at skeletal maturity (when growth plates close and bones don’t grow any longer) have been reported to weigh from under 15 pounds to slightly over 30 pounds. Normal weights for GSD bitches are 55-75 pounds, and for males 70-90 pounds. It’s not unusual for a bitch to give birth to ten pounds of puppies, plus carry the extra weight of fluid and placental tissue. For a dwarf bitch, that percentage would be impossible, I would think.
The variable size of the pituitary dwarf Shepherds reported so far is an indication of the possibilities that the trait itself could be a threshold polygenic trait (unlikely), but the variation could also result from modifier genes governing varying time of growth cessation. There are some differences in absence, presence, or level of growth hormone in untreated dwarfs, and those that grow to be larger than others before the growth plates close may simply have more GH. Since the “problem” has been swept under the rug so often, and is rare enough to begin with, professors at veterinary colleges are in disagreement over the meager information that is available. Thanks to the breeder in Arkansas, several universities and the Morris Animal Foundation were currently studying the data and the dogs.
This type of pituitary dwarfism involves the German Shepherd Dog, but a breed from the Russia-Finland border, called the Karelian Bear Dog, is also affected. The reason is that the Karelian (Finnish spelling is Carelian) has the GSD as part of its ancestry, and the affected individuals had some GSD carriers in their pedigrees. The scientific literature has reported one Yorkshire Terrier, one “Toy Pinscher”, and two “Spitzes” as well, but it is highly doubtful that those are the same genetic defect. If I find several examples, as there are in the GSD, I’ll withdraw my doubts.
Fred Lanting is a German Shepherd Dog breeder, judge, and breed authority, and is the author of books on Canine Hip Dysplasia and Other Orthopedic Disorders (www.MrGSD.com), and The Total GSD (www.hoflin.com). He lectures around the world on canine orthopedics, and structure and gait. Articles are found on many websites, and permission can be requested at <mrgsd@hiwaay.net>.
WUSV-SV Rules for BH and SchH-VPG-IPO, Levels 1, 2, & 3 Translation & Š 2004 by Fred Lanting
Part One: The 2004 SV/WUSV/FCI Rules for the BH Qualification
COMPANION DOG AND BEHAVIOR/TEMPERAMENT TEST, WITH TRAFFIC SURENESS AND OTHER SPECIAL EXPERIENCE
(Begleithund & Verhaltens Test, BH/VT; sometimes simply called “B”)
All examinations and qualification events are subject to principles of sportsmanship regarding the performance and behavior of those involved. The execution, demonstration, and evaluation are more thoroughly described below. These regulations are binding for all involved, and all participants have to meet the same performance requirements. One change is that at the BH/VT examination, the gunsureness test no longer takes place. In order to participate in FH, SchH/VPG, IPO, RTP (SAR), Agility, and Obedience events, proof of the BH/VT is required. Authorized to award the BH/VT are SchH/VPG, Agility and Obedience trial judges listed and approved by any AZG-member association. The examination result is to be noted in the appropriate performance record, such as scorebook or Ahnentafel (pedigree/registration paper). Minimum ages are at the end of this article. Continue reading
SV Standard – translated by Fred Lanting
FCI Standard #166; Adopted 1997; replaces 23 March, 1991 edition
(Dentition change added January 2002)
FCI Classification: Group 1 – Guardian and Driving dogs;
Section 1 – Shepherds’ dogs with working titles.
Versatile use: Guardian and Service (Working) Dog
Short historic overview:
Since the official establishment in Augsburg, within the German Canine Association known as the VDH (German “Kennel Club”), the parent club of the breed, the Club for German Shepherd Dogs (SV), is responsible for the breed Standard of the German Shepherd Dog. The Standard was set up in the first membership meeting in Frankfurt on 20 September 1899, upon the suggestions of A. Meyer and M. von Stephanitz, and then revised at the 6th membership gathering on 28 July 1901, the 23rd meeting in Köln on 17 September 1909, the conference of the executive committee and board in Wiesbaden on 5 September 1930, and the breed committee and board of directors meeting on 25 March 1961. As part of that one, the World Union of German Shepherd Dog Clubs (WUSV), was involved with the work. At the WUSV conference on 30 August 1976 they agreed on another revision, and on 23/24 March 1991 assumed full powers by way of resolution of the executive and advisory committees. [The current version was adopted in 1997.] Continue reading
Breed Show (SV Conformation Show) Rules, Germany – 1997 version, translated by Fred Lanting
The following rules are enforced in Germany, and offered as a guide to other countries’ clubs.
Breed Show (SV Conformation Show) Rules, Germany
1997 version, translated by Fred Lanting
The club for German Shepherd Dogs (SV) is the parent club of the breed, acknowledged by the VDH and the FCI. For the purpose of the conservation and further development of the breed, the statutes of the SV (delineated at SV headquarters for SV member-clubs) generally and in particular for the handling of the organization, indispensable for the breed, the SV gives the following “breed show rules”. These regulations are to have the effect of law (for members). Continue reading
The 2004 SV/WUSV/FCI Rules for the BH Qualification (Translated into English by Fred Lanting)
The 2004 SV/WUSV/FCI Rules for the BH Qualification
Translation copyrighted by Fred Lanting
COMPANION DOG AND BEHAVIOR/TEMPERAMENT TEST, WITH TRAFFIC SURENESS AND OTHER SPECIAL EXPERIENCE
(Begleithund & Verhaltens Test, BH/VT)
All examinations and qualification events are subject to principles of sportsmanship regarding the performance and behavior of those involved. The execution, demonstration, and evaluation are more thoroughly described below. These regulations are binding for all involved, and all participants have to meet the same performance requirements. One change is that at the BH/VT examination, the gunsureness test no longer takes place. In order to participate in FH, SchH/VPG, IPO, RTP (SAR), Agility, and Obedience events, proof of the BH/VT is required. Authorized to award the BH/VT are SchH/VPG, Agility and Obedience trial judges listed and approved by any AZG-member association. The examination result is to be noted in the appropriate performance record, such as scorebook or Ahnentafel. Continue reading