Monthly Archives: July 2008

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 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:
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.



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” ( 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.




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 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.



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.




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 called, 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, , 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 (, and The Total GSD ( He lectures around the world on canine orthope­dics, and structure and gait. Articles are found on many websites, and permission can be requested at <>.


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