Articles written by Fred.

Common Sense Grooming Part 3 – Teeth and Nails

It always disappoints and dismays me as a dog-show judge to examine dogs in the ring and find some of them filthy (which very seldom happens) or many with neglected teeth (which happens regularly — even in the majority of cases, in some breeds such as the GSD). Without good, home dental care, they teeth may recede into swollen gums with gingivitis, or they may even fall out by the time the dog is nine or ten years old. It’s as if the owners think, “Well, the dog will only last that long or a little longer, so why bother?” While it is true that dogs wear down or break off their teeth by about the time they will soon no longer need them, there is no excuse for ignoring the dog’s need for regular cleaning to the point that we cause him to reach that stage years before the natural consummation of his life. To rely on dry dog food to scrape tartar off the teeth is no different than to rely on exercising your jaw muscles by eating only corn flakes with milk. Continue reading

Common Sense Grooming Part 2 – The Clean Dog

During or following the semi-annual major hair loss, you can bathe the dog, if he still needs washing, with a good pH-balanced shampoo especially formulated for dogs. Baby shampoo will do as well, and as long as you don’t wash him too frequently, plain old hand soap is good enough. Bathing will help loosen and remove much of the rest of the dead hair. This is especially helpful if you don’t take time for daily prolonged combing during these shedding periods. Have the dog lie on the concrete run or wooden porch, soak him with water from the hose, then work in shampoo or bar soap until you get a good lather, rolling him over to get the belly and other side, then the head and neck. Hold the head almost all the while, or the dog will struggle to get up and shake. After he is soaped from ears to tail tip, let him up to run around for about five minutes while the dirt is emulsified and any ectoparasites are drowned (fleas and ticks will survive under plain water, but cannot breathe in soapy water). By the way, I don’t believe the flea shampoos are any more effective than just letting the dog’s coat stay soapy for several minutes. Continue reading

Common Sense Grooming Part 1 – The Haircoat

Fred Lanting

“Show me your dog, and I will tell you what sort of man you are.” …von Stephanitz, 1932

Although it is a characteristic of the German Shepherd Dog (which I have bred and judged almost since they walked off the Ark), the double coat is not unique to this breed, and the grooming techniques I have found to be best (and which I describe here) are applicable to many breeds. For readers who have terriers, sighthounds, poodles, and some others, you’ll have to modify these tips. The soft, fluffy undercoat of many scores of breeds is very light and somewhat flyaway, while the topcoat is coarse, heavier, usually straight, and imbeds itself like a whipworm into woven fabric, snaking in and out of the warp to defy your best efforts in brushing. Your Whippet’s coat may be a lot shorter than your Saint Bernard’s, but there are more similarities than differences once you realize that, at the same cut-short length, the hairs are of almost all dogs are of the same types. Tightness of curl just throws another characteristic into the recommendations for coat care. Classifying haircoat types on the basis of length, the German Shepherd Dog’s is considered to be “normal” or intermediate, compared to the short hair of the Boxer and the long hair of the Newfoundland. 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. Continue reading

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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Most worms (nematodes) settle and grow in the small intestine, though some species are found in the cecum, heart, lung, and other tissues in various stages of development. The intestinal nematodes produce eggs, which are carried with the digestive products to exit in the feces. But since the egg-lay­ing does not always coincide with the dog’s bowel movements, stool samples may not show the presence of worms. A 5?day sampling will probably reveal some eggs if hookworms or roundworms are present, but tapeworms or whipworms may still escape detection. For this reason, many breeders rely instead on outward signs of poor coat, flatu­lence and/or diarrhea, loss of weight, and an abnor­mal look or smell to the stool.

In many breeds, the topcoat should lie flat, straight, and smooth, giving a water?resistant thatch over the softer undercoat and skin. If these coarse, straight guard hairs stand up and out, or if the ends curl out away from the body, it may be a temporarily “open” condition due to worms. Lustre and texture also is gone, and the feel is rough and dry, the natural lubrications being lost when worms take their tariff from the intestinal lining’s rich supply of blood vessels, or otherwise interfere with normal absorption of nutrients. In this article you will see the word anthelmintics, which is the more accurate word for “wormer”, “worm medicine”, etc.

Roundworm — This is the most widespread of parasitic worms in dogs, cats, and many other animals. They are present in almost all newborn pups, having passed in larval stage through the placenta into the fetus’s liver. After birth, these larvae are carried by the blood to the heart, then to the lungs. Irritation of the bronchial passages causes the dog to gag and cough the larvae up, then swallow them. This enables the larvae to reach the intestines where they latch onto the walls with lamprey-like tenacity, and in as few as ten days can be found to have matured into identifiable round­worms of egg?laying capacity.

Older pups that get worms a second time usually do so by ingesting worm eggs from stool or stool-­contaminated surfaces. Pups (and adults) may also pick up roundworms from cat stools, which present a tremendous attraction. Larvae have also been detected in bitch’s milk. Swallowed roundworm eggs hatch in the intestine where the liberated larvae penetrate the wall and are carried in the lymph system to the veins. They, too, take the liver?heart-­lungs route, molt, and start laying eggs of their own four weeks after being ingested. So, it’s a good idea to repeat initial worming a couple weeks later, whether it’s a new litter or a dog you have just obtained but aren’t sure of its worming history (such as may be the case with some imports).

Adults and half?grown dogs tend to trap some roundworm larvae in body tissues in an encapsulated or encysted condition, where they do no further harm. Pregnant bitches, however, undergo a hormone change about three weeks before whelping that releases the encysted larvae, freeing them to migrate to the placenta and affect the fetuses as the bitch herself was affected when she was a growing embryo. This dormant stage of roundworm larvae can also exist in transient or intermediate hosts such as rodents, and if mice are eaten, the process of digestion will release the larvae in the dog’s intestine, where they will not migrate (because they are in a different form), but develop into roundworms. Dogs that catch and eat beetles, cockroaches, mice, even earthworms, all of which may be hosts for roundworms, should periodically be given anthelmintics (wormers) as a routine control measure. Pyrantel pamoate (Strongid™, Nemex™) is an excellent anthelmintic for the youngest puppies because it is considered non-toxic and very safe even if rather overdosed accidentally; it is highly effective against round and hookworms. A good routine is to administer 2 weeks after birth, and then again 10 days after that. The next worming can be with ivermectin, but if you have a very small breed, you might want to dilute that. More on this anthelmintic drug later.

Hookworm — Hookworms are much smaller than roundworms and cannot be seen outside the dog, but as in the case of roundworms, eggs can be detected in fecal matter under the microscope. “Hook”, as dog fanciers often call it, is a debilitating disease in adults and a frequent killer of pups. It is possibly the leading cause of death in puppies over two or three weeks of age. In chewing their way to blood vessels serving the intestinal walls, hookworms inflame the lining and make the organ less efficient. As a result, the dog becomes malnourished as well as anemic. Bloody stool, diarrhea, anemia, weakness, and dehydration are symptom of hookworm infestation, in addition to the sign of poor coat condition. There are a number of good anthelmintics, but the one I find most convenient, safe, and effective is ivermectin, good not only for heartworm prevention, but also for preventing and treating for round, hook, whip, and even ticks. Interceptor™ (milbemycin) is another heartworm “medicine” that gets many of these parasites. Since all wormers are potentially dangerous especially to debilitated pups, follow your veterinarian’s orders when worming sick or very weak pups. Hookworm can commonly be picked up at dog shows, veterinarians’ lawns and lobbies, city sidewalks, and parks where dogs defecate. The eggs can live a long time in the soil, but sunlight helps to kill them, and full?strength chlorine bleach can destroy or force them to hatch and thus be susceptible to attack by products available from your veterinarian.

“A whip so small you could not see it, I’ve known to lash the mighty creature till it fell.”

…Emily Dickinson, 1874

Whipworm — Whipworm infestation is usually less of a problem since it is not so widespread, but it’s harder to detect and eradicate. Eggs are extremely resistant to the environment, and larvae can exist for several years in the soil or cracks in basement floors. Whipworms don’t lay as many eggs, or as often, as other worms, so they are more difficult to detect. Take several days’ stool samples (in one mixture) to the vet. Symptoms are similar to those of hook, and repeated doses with specific whipcides are quite effective when strict sanitation is an adjunct. Generally, anything that will kill hookworms or whipworms will also kill roundworms but it might be a longer battle before you are feeling safe. Febantel has generally replaced the old dichlorvos (Task™, Atgard™) as the wormer of choice. Dichlorvos once was widely used for whip, hook, and roundworms as well as a ingredient in impregnated-plastic strips for fly control, but was a bit risky for the youngest pups or dogs with liver or kidney insufficiency or heartworm, or if absorbed along with other cholinesterase inhibitors.

So the lone Taenia, as he grows, prolongs His flatten’d form with young adherent throngs.

…Erasmus Darwin, in The Temple of Nature, before 1800

Tapeworm — A variety of tapeworms (cestodes) infest dogs and all of these flatworm parasites rely on an intermediate host in order to be transmitted from one direct host to another. Depending on the genus and species, some require an insect, others a crustacean, still others a different mammal in which they exist in a non-worm stage such as a larva, usually encysted. Eggs are seldom detected in flotation slides, but the owner may see little white crawling things on the surface of some stools. These are called proglottids, segments of the tapeworm that contain the eggs and are shed by the worm in order to propagate itself while the head and younger segments remain attached to the inside of the dog. The shed segments have been likened to rice grains, cucumber seeds, and tiny blunt arrowheads and can vary in size from those of cucumber seed dimensions down to nearly microscopic particles that can be mistaken for frost if seen on a cold morning. The stool is not necessarily soft, unless the infestation is so bad that diarrhea is around the corner. However, tapeworms should be suspected when the dog has been wormed for hook yet still has flatulence and poor coat. He must then have the specific tapeworm anthelmintic.

Dipylidium caninum, a member of one of the most common flatworm parasite groups in dogs, is transmitted by the dog flea and the cat flea. When the dog bites and eats the flea, the tapeworm larva is given access to the canine intestine where the cycle starts again. The flea’s family members, meanwhile, are waiting in the grass (or even your carpets!) to feed on the eggs in the proglottids shed by earlier tapeworms. The genus Taenia includes several species of tapeworm, the most common of which is T. pisiformis. Most cases of infestation come about when the dog eats a rabbit or mouse in whose intestines can be found encysted Taenia larvae. Prevention of infection with Taenia includes not allowing your dog to eat raw wildlife, particularly the internal organs, and especially rodents. The best preventive measure against Dipylidium is to keep your dog from socializing with cats or visiting places where cats hang out, for our feline friends are typical intermediate hosts even though they are seldom bothered by the fleabites.

A much-used wormer called praziquantel (trade name Droncit™), is nearly 100 percent effective against both of the above types of tapeworm. It causes the tapeworm to lose resistance to digestion by the host, so you will rarely see pieces of the worm in the stool after the wormer has done its job. Other anthelmintics for hookworms, roundworms, and whipworms don’t affect either of these tapeworms. A few minor flatworms are transmitted by the eating of raw fish. Another species, Echinococcus granulosus, is a danger to man, its intermediate host. It is found mostly in Alaska and parts of Canada. There is a tablet anthelmintic sold under the trade name “Drontal™ Plus” which combines Droncit with pyrantel pamoate (the latter paralyzes hook and round worms). There is also febantel, which interferes with the metabolic process of whipworms; a combination with praziquantel is useful in the control of several types of intestinal worms with one dose. Some of these can be also be administered by injection.

Other worms — I have limited these suggestions to worm problems that are most common in North America. There is insufficient room or reason to describe the other, much more minor, worms that can bother dogs in this region, but if your dog exhibits typical “wormy” symptoms and a couple of routine wormings a few weeks apart don’t improve his condition, take a 5?day stool sample into the veterinarian for a complete study.

The changing scene — Wormers, like flea and tick killers, are constantly in a state of flux, so make sure your vet and you keep up to date on the latest studies. But don’t automatically assume that if something new is highly effective, that it is the best. Many old and relatively safe approaches can still be used. Telmin™ (mebendazole), Scoloban™ (bunamidine), DNP, Vermiplex™, and Styquin are effectively off the market in the USA now. Wormers similar to Vermiplex may kill a fairly high percentage of hookworms, roundworms, and considerable numbers of tapeworms, but not enough to completely eradicate an infestation; many of these are principally toluene or similarly offensive solvents. They usually require fasting before effective administration.



Product: Hook Round Whip Tape
Ivermectin* +++ +++ +++  –
Pyrantel (Nemex, Strongid)** +++ +++ – 
Fenbendazole (Panacur™)*** +++ +++ +++ ++(Taenia only)
Dichlorvos ++ ++ ++
Praziquantel (Droncit™) –  –   – +++
Drontal-Plus (prazi- & pyr. pam.) +++ +++ +++ +++
Milbemycin (Interceptor™) ++ ++ ++
Paracitide-10™ (prazi- & febantel) +++ +++ +++ +++

*When packaged for cattle and sold in feed stores without prescription. Ivermectin had long been sold “off-label” for dogs; it has been considered dangerous in Collies, Shelties, and crosses of these, if given in doses large enough for treating intestinal worms.

**Pyrantel pamoate is also sold as a paste for horses, but dividing doses of that form is difficult; the pleasant-tasting liquid sold for dogs is easiest to administer, though tablets are also available. For hookworm, which is hard to rid from the premises, every other week for 6 weeks may be required. Better to switch to ivermectin after the first dose.

***Panacur is effective against only one type of tapeworm (Taenia, not Dipylidium); it is administered for 5 days for the tapeworm and 3 days for other worms.


In all cases, it is wise to treat the dam 2-3 weeks after whelping, or after her pups start eating “solid” food in the last stage of the weaning process. I have found that almost all intestinal worm problems seen in North America can be prevented by initially dosing pups when they are 2 weeks old with Nemex, effective against canine roundworms and hookworms, and then start oral ivermectin another two weeks after that. For both worms and ticks, I use Ivomec™ (a brand name, and labeled “for cattle and swine”), purchased at feed stores in 50-ml bottles of 1% injectable ivermectin (it’s the active ingredient in Heartgard™). Sold there for cattle & swine, the same stuff takes care of various worms in the canine. One bottle will possibly last most of a little dog’s life, but even with large breeds, you won’t be spending the small fortune that others do. I store mine in the refrigerator, even though there doesn’t appear to be a shelf-life problem at room temperature. It’s up to you (and maybe your vet, if you wish) what you choose, but I have had good results for many years with the protocol I describe in this article.

The Heartgard dosage to prevent heartworm, as I once wrote down from their old literature, is 6 micrograms per kilogram of body weight. But buying the high-priced pills from the vet is too expensive for my tastes, when I get the same results by shopping where the livestock farmers shop. The insert in the package of 1% Ivomec recommends one milliliter (1 ml = approx. 1 cc) per 110 pounds of bovine, and 1 ml per pound of swine. Anatomically and medically speaking, dogs are more similar to pigs than to cows, so I chose the swine dosage as a starting point. Equivalents in medical jargon are 200 and 300 micrograms per kilogram of body weight in cattle and swine, respectively, both much higher than what I use monthly.

The insert explains that ivermectin’s “wide margin of safety [in mammals] is attributable to the fact that… [the active ingredients, lactones]… do not readily cross the blood-brain barrier. In other words, the chemical/drug acts so much more on the brainless parasite than on your smart, “brainy” dog. In cattle and swine, the Ivomec insert says, ivermectin is effective against gastro-intestinal worms, lice, and mites.

Some people ask, “Can I figure out the dosage from the label on the bottle?” Yes, but is it necessary? You may have to do a lot of converting of volume measurements, metric system designations, etc. What others use (it already has been done for you) may be close enough, as long as you feel comfortable with its use in your breed. I have had many years of success, treating my GSDs, Shibas, and Whippets with never a sick dog because of ivermectin.

I dose orally, not by injection, even though I buy the “injectable” form from my local farm supply & feed store. You should understand that less of almost any drug gets into the circulatory system if ingested, than if injected. Keeping that in mind, the manufacturers’ suggested levels (designed for hypodermic injection) are usually a good bit below what they probably would recommend for oral administration.

Heartworm — Only mosquitoes apparently can incubate the heartworm nematode, and only certain species of mosquito seem willing to do the job; unfortunately, they seem to be everywhere. Reportedly, foxes as well as coyotes can keep the problem alive in any given area, but there are enough dogs around that are not on a preventative, that they don’t need any help from wild animals to spread this disorder. A good blood test can uncover microfilariae. An old control measure once used in some parts of the South was the twice?yearly treatment with “arsenic” (thiacetarsamide), to kill adult heartworm. A newer, far less harsh, and far superior preventative is the once-a-month dosage with either ivermectin (most common trademark as sold by vets is Heartgard™) or milbemycin (sold as Interceptor™). Ivermectin was long used by farmers as a cattle wormer; they found it got rid of all worms (except tapeworms) in their dogs, too.

The lifecycle of the heartworm begins with the mosquito feeding on an infested dog. It picks up, with the blood, some tiny heartworm embryos called microfilariae. Within minutes, the microfilariae begin to migrate from the gut to another part of the mosquito, changing into an infective form called larvae. In a couple of weeks these larvae move to the mosquito’s mouth and when the insect bites the dog they escape into the blood, fat, and mucous tissues of that victim. There they continue to develop in the fatty tissue under the dog’s skin and undergo more molts. In a few weeks they enter the veins as immature worms and reach the heart three months after entering the dog. Growing to a length of some seven inches for males and almost twice that for females, they lodge in the heart, copulate, and produce eggs that then hatch into microfilariae, and the cycle is complete.

The danger to the dog is in the worms’ interference with flow of blood, proper opening and closing of the heart valves, effective oxygenation of cells, and proper blood flow to the lungs, especially when the worms die and clog up the pulmonary arteries. The principal danger to the dog with an adult heartworm population being treated with arsenic is when the dead worms let go and obstruct the pulmonary arterial flow; pneumonia is then the most likely cause of death, so the dog must be kept from exercise or exertion during this treatment period.

For heartworm prevention, I aim for approximately 0.15 ml for every 50 lbs. of dog body weight, 0.21 ml for 75 lbs., and 0.27 for 100 lbs. Naturally, you can’t be accurate to two decimal places, even when you use a 1-ml “TB” syringe, but I don’t have to be precise, as it is quite a safe drug for almost all breeds, especially at this low preventive/maintenance level. I dose once a month, and I don’t worry about giving a little more than the above amounts. I don’t even do stool checks any more; just use that dosage as a prophylactic (preventive) approach. Almost any diabetic can get a hypodermic syringe and needle for you.

For actual round-, hook-, or whipworm presence, or high exposure risk such as weekly exhibition on probably-contaminated dog show grounds, I give my dogs a higher dose: 0.3 to 0.4 ml per 25 lbs., or 1 ml per 75 lbs. every 4 or 6 months instead of their regular low-dose level. I also use the higher dose to combat ticks when they get especially bothersome.


While I still maintain that the best way to control ticks is to go over your dog every day and pluck them off with a tweezers and drown them in soapy water (or other detergent), you can also get an additional measure of control by using ivermectin. Especially if you have an unusually bad tick year. Higher doses than I use against worms are used in Australia as a public health measure in rural Aboriginal communities (where the children and some of the adults sleep and otherwise are in intimate contact with their crossbred dingoes) to kill ticks and sarcoptic mites on family dogs. There it has been found that dosing every six weeks was adequate in controlling the tick problem on both the pets and their owners. In that country, the use of ivermectin as a public health measure has favorably affected mortality rates of both man and dog, and greatly improved the health of both. When the dogs are made tick-free and cleared of Sarcoptes, the children benefit because they no longer contract these diseases from their furry friends. There is much history elsewhere of using it for mites & ticks. In much larger, more frequent long-term doses, it has been used against demodectic mange. My personal experience, verified by anecdotes from others, is that ivermectin has considerable action against ear mites and ticks (which are non-insects) but not against fleas (insects).

The higher de-worming level I mentioned earlier is what I also use (in alternate months or two to four times a year) when ticks get bad (as in 2007 and 2008 when we in northern Alabama saw the third-worst tick problem in 30 years). Or else, I’ll give the dogs an extra mid-month (roundworm-control-size) dose, and that helps control the ticks a great deal. The nasty little arthropods still bite, but very few survive long enough to suck much blood. They tend to “die and dry”. By the way, this “large dose” (as I call the one I give for other than heartworm preventive), is the same that pigs get by injection. And as I said, not as much gets absorbed through the gut as would if injected subcutaneously.

Procedure: I stick a 1-ml “hypo” (the size used by diabetics, and what used to be called a “TB syringe”) into the rubber-stoppered 50-ml bottle. The first of the month, I pull the desired amount into the barrel, disconnect it so that the needle stays in the bottle (stuck in the rubber seal), and squirt the selected volume into the mouth of the dog.
The website

has more on efficacy of medications like this. This information is not a medical recommendation; by law in most states, you need to confer with your veterinarian for that.


Owners of certain at-risk Collies, Shelties, Sheltie mixes such as Silken Windhounds, perhaps Australian Shepherds, Kelpies, etc. might want to check current knowledge on vet websites for information on “the mdr1 mutation”. As the moderator of a veterinary medicine Internet chat list says, “Mixes of unknown pedigree should be treated with caution at the higher ivermectin doses.” Which higher doses, you may ask? Well, that’s a reference to using the drug for killing intestinal worms, not the level for heartworm control.

Well-versed and careful researcher John Cargill says, “Moxidectin (in Proheart™ tablets) is given once a month to prevent heartworm disease. [Several] products contain macrocyclic lactones which kill the tissue stages of heartworm larvae and are given once a month. They are generally very safe, but should not be used in young pups as they can enter the brain and cause nervous system symptoms such as depression and signs of stupor. Collie-type dogs are more sensitive to nervous-system effects than other dogs, but even in these breeds, the products are safe at recommended doses.”

Bonnie Dalzell, Borzoi breeder and another respected data researcher, says: The dose I got from a vet working for Merck, using the 1% liquid “horse Ivomec”: for dogs who do not have the MDR1 gene, 1 cc orally for 135 lbs of dog; the heartworm prevention dose, safe for MDR1 dogs: 0.1 cc orally per 135 lbs of weight. I do not try to get an accurate low heartworm dose for a 10-lb. dog — I would use the Heartgard or Interceptor instead. Breeds that have been shown to have around 30% individuals with the MDR1 gene include Silken Windhounds (Whippet cross, probably with Sheltie), Shetland Sheepdogs, Rough Collies, and Australian Shepherds. If you are in doubt, there is now a PCR test for this gene. Since you can test to find carriers, you could even eliminate it from a lineage of dogs. Here are two abstracts:

In case you have not heard of that gene Bonnie talked about, here is a news item from late 2007:


“When given a high dosage of ivermectin heartworm medication, many Collies developed severe neurological signs that often resulted in death due to respiratory arrest. Statistical data on drug sensitivity included Collies, Australian Shepherds, Bearded Collies, Border Collies, Shetland Sheepdogs, etc. and drugs ranging from an over-the-counter anti-diarrhea medication (Loperamide) and pain controller Butorphanol to some chemotherapy drugs. The mystery has finally been solved. A recent study by Dr. Katrina Mealey has identified that the problem of drug sensitivity relates to a genetic mutation in the multidrug-resistance gene (MDR1). One of the responsibilities of the gene MDR1 is the production of a protein called P-glycoprotein (P-gp). This protein allows many toxins and drugs to be removed from the brain. An affected dog lacks functional P-glycoprotein that leads to toxins not being pumped out of the brain and, as a consequence, to an abnormal neurological reaction. The mutation has an autosomal recessive way of inheritance which means that, in order to be affected (super sensitive to drugs), a dog has to have both genes mutated. However, even the presence of a single mutation increases drug sensitivity in a dog. A new DNA test for the presence of the mutation MDR1 gene allows for the detection of affected dogs as well as dogs carrying a single mutation. Knowing the dog’s status will help veterinarians to properly administer treatment and will help breeders to eliminate this disease in their bloodlines. To learn more about ordering the test, see


Ivermectin vs. other drugs:

Here, as additional information, is a collection of some of the statistics on adverse effects of the various heartworm preventatives currently on the market. The data in the following list was compiled from the Food and Drug Administration listing of Adverse Drug Experience Reports, <> The number of deaths per year is significant, although comparative percentages are not given. Selected other adverse events are also reported.

Ivermectin, Oral, Dogs (Heartgard & other brands) Year approved: 1987

Number of Adverse Drug Experience (ADE) Reports in FDA through 7 June 2007: 1,069 (per year: 53)

Total Deaths: 126 (6 per year since FDA approval); Anemia: 6; Platelets low: 3; autoimmune hem: 3

Reports of ineffectiveness against heartworm: 10 per year


Ivermectin & Pyrantel combination, Oral, Dogs (Heartgard Plus): Year approved: 1993

Number of Adverse Drug (ADE) Reports in FDA through 7 June 2007: 9,871 (705/yr)

Total Deaths: 97 (7/yr); Selected other adverse events reported: Convulsion(s): 197; Anemia: 25; Autoimmune hemolytic anemia: 20; Platelets low: 9

Reports of ineffectiveness against heartworm: 156/yr


Milbemycin, Oral, Dog (Interceptor™ brand name) Year approved; 1995

ADE Reports in FDA through 7 June 2007: 4,745 (395/yr)

Total Deaths: 159 (13/yr); Convulsions: 268; Anemia: 29; autoimmune hem: 15; Platelets low: 1

Reports of ineffectiveness against heartworm (total): 2757

Ineffective against heartworm reports per year: 230


Milbemycine oxide with Luferon, Oral, Dogs (Sentinel™): Year approved: 1995

ADE Reports in FDA through 7 June 2007: 1,777 (148/yr)

Total Deaths: 43 (5/yr); Convulsions: 109; Anemia: 10; autoimmune hem.: 8; others: 4; Platelets low: 12

Total reports of ineffectiveness against heartworm: 775 (65/yr)


Selamectin, Topical, Dogs (Revolution™) Year approved: 1999

ADE Reports through 7 June 2007: 10,917 (1,365/yr)

Total Deaths: 217 (27/yr); Convulsions: 339; Anemia: 60; Autoimmune hem: 16; Other anenmia: 37; Platelets low: 59

Total reports of ineffectiveness against heartworm: 3,855 (481/yr)

Selected other ineffectivness reports: fleas: 1,622; ticks: 501; ear mites: 206; mites: 61; sarcoptes mites: 56; other ectoparasites: 11; treating for hookworms: 11; hookworm prevention: 45. Selamectin lufenuron* is a once-monthly topical liquid applied to the skin at the back of the neck and sold as a preventative for heartworm and to control fleas (by preventing flea eggs from hatching, but it does not kill adults) plus sarcoptic and ear-mites in dogs. Revolution has about 4 to 5 times the fatality rate of other wormers.
* Luferon, lufenuron: Lufenuron is also sold under the brand name of “Program”. Lufenuron is an insect egg killer; will not work on adult nematodes, it is said. It is sold by dog weight. The active ingredient is Luferon and is promoted as a “flea contraceptive” — prevents fleas from successfully breeding but does not kill adult fleas. Program (Lufenuron) and Sentinel (Luferon/Mibemycin Oxime) break the reproductive cycle by preventing flea eggs from developing. Sentinel also kills heartworm larvae, adult roundworm, hookworm and whipworm.

I hope this has been helpful to you in the management of your dog’s health. For much more on caring for your dog, whatever breed, I suggest you order the following:

Canine HD and Other Orthopedics Disorders” ISBN 0-9764685-0-6 Copyright 2005 by Fred Lanting

In the bright blue cover signifying the second printing, it’s the long-awaited, expanded revision of the popular HD book (the first one, published in 1980, sold 10,000 copies!). This book is a comprehensive (nearly 600 pages), amply illustrated, annotated, monumental work that is suitable as a coffee-table book, a reference work for breeders and veterinarians, and a study adjunct for veterinary students. It is equally valuable for the dog trainer and the general dog owner of any breed, as there is no breed that does not have some sort of orthopedic, bone, or spinal disorder. Do not confuse it with the out-of-print 1980 work, which was much smaller. This new book covers every aspect of HD and most other disorders, and includes genetics, diagnostic methods, treatment options, and the role that environment plays. US $68, plus $5 postage in the U.S., or $** for surface mail overseas. (Ask about international shipments): e-mail or write to Willow Wood, 3565 Parches Cove, Union Grove, Alabama 35175-8422 USA. Volume discounts for clubs and resellers. The author has been studying and teaching this subject since 1966, including lecturing at numerous veterinary schools and breeders’ convocations in some 30 countries throughout the world. He has been described by a former OFA director as the world’s leading non-veterinarian authority on hip dysplasia. He has been a dog breeder since 1945, a GSD owner since 1947, and a show judge since 1979.

Combine orders with “The Total German Shepherd Dog” by the same author ($50 plus postage). 17 of the 20 chapters are suitable for owners of any breed. Search my name on Google for magazine and website articles. Permission to quote brief excerpts is allowed; otherwise no part of any work may be reproduced without prior written permission from the author:


Will the True Working Dog Disappear Part 2 – The Gap Widens

by Fred Lanting

In the German Shepherd Dog world, and echoed elsewhere, we have long heard (and voiced) complaints about the schism that exists between the “show” (Hochzuchtlinie or high-breeding) lines and the “sport” or working-competition (Leistungs) lines. I’ll speak to the issue of the non-standard (AKC, Alsatian) styles elsewhere, but first I intend to discuss the continued and even widening gap in the international type. Here, I will allude a little more to the history of the breed. You might consider this “Part Two”, with an illustrated companion article (though not actually designated “Part One”) having been made available under the title, “Will the True Working Dog Disappear?”

The vision of Max von Stephanitz, which even today is cherished by many of us who love the breed, was to standardize, to “fix Type” in, the many variations of the shepherd’s dog he found all over Germany and many adjoining lands. Some were shaggy, others were short-coated. Some were scrawny, some high in the rear, some had ears that did always stand up. But all that he incorporated into the new “breed” association in 1899 had jobs they worked in.

Besides the flock tending, which was becoming less needed in the age of industrialization and migration to the cities, dogs with these talents and type were finding other occupations. Captain von Stephanitz saw, selected, and developed the abilities that soon made his German Shepherd Dog the preferred breed for police and military service. Before long, its combination of sensitivity and need for nearly-constant human contact, plus its size, made it ideal for the newly-recognized occupation of guide dog for blind people. It was still a dog with “working papers”.

Between the two big wars, the pastime of exhibition and competition grew, designed to select the dogs that looked like they were best qualified to produce the next generation. Coat length and colors, body size and proportions, ear and tail carriage — all these were added to the evaluation of character and some evidence of utility. Conformation competition classes were categorized by age, with any dog over two years old being required to have a suitable training title in order to compete in the “beauty” shows. These titles included the HGH herding certificate and the newer Schutzhund (protection) title. Other, less-encountered service designations were retained for a while.

After WW-2, with the breed in Germany decimated as a result of personal dogs having been commandeered by the military, and most of them killed in action or having disappeared when the concentration camps were found and dismantled, the breed and sport had to start all over with a limited gene pool. Conformation shows were only suspended during a few of the war years. Still, despite different zones of Germany being assigned to the major allies, and many GSDs becoming prisoners of Communism behind an iron curtain, there was still the oneness of the breed, with one conformation standard and set of requirements for proof of working ability.

This united, single-breed status continued for another couple of decades. In Eastern Europe, because of the Soviet Union’s cancellation of such freedoms as communication, dogs on “their side” stopped sharing and exchanging genetic material with their western counterparts. Therefore, we who were around then and for many years later could see the result of this isolation. We could spot, at a glance, the rust-red Czech dog, the bicolor or black East German dog, and the wiry sables from many parts of these imprisoned lands. But in western Germany and in all the countries of the free world that got dogs from there, the GSD looked pretty much the same. Even in North America, where no proof of working ability was or is needed, the international type and styles were honored until the late 1960s.

There are two main annual, national competition events in Germany that are of the greatest interest to people around the world, and I have led tour groups to both. One is variously called the Sieger Show or Bundessiegerzuchtschau (BSZS), and the other is the Bundessiegerprüfung (BSP). The former, held around the first of September, is supposed to select and rank those dogs that conform anatomically, and the latter is to rank those that perform all the schutzhund exercises (tracking, obedience, and protection). The BSP is generally held two weeks after the conformation event, in a different part of Germany. The BSZS is open to all qualified dogs regardless of country of birth or residence, but the practical fact is that if a dog has not been competing in Germany’s local and regional shows during the spring and summer under the judge who will see them at the Sieger Show, and if it has not been placing highly there, it will not get an elevated placing at the big show in the autumn. The BSP is open only to dogs resident in Germany.

At the Sieger Show, there is a qualification performance for adult dogs on the first of the three days. It is commonly referred to as “the courage test” and involves two short excerpts from the SchH-1 (IP-1) exercise. In the first one, the handler and dog walk at heel toward a blind from which an attacker jumps out and threatens them. In the second, the dog is sent from the far end of the field to intercept the “bad guy”. In each case, the trespasser is charging at them, waving a stick as his weapon. The dog must confidently and firmly hit the intruder, and bite steadily with (hopefully) a full-mouth grip. The dog must not “shy” at any time or let go during the struggle.

In each case, after the “out”, the dog must guard the motionless “bad guy” until picked up by the handler. An evaluation of Ausgeprägt (pronounced) enables a dog to be presented for the conformation judging, which for that dog begins a few minutes after leaving the courage test field. An evaluation of Vorhanden (sufficient” means the dog barely passed but with a relatively poor level of courage and fighting drive (TSB). Such a dog can still get an SG (Very Good) rating at most, but is ineligible for the V (excellent) rating, or the VA, which is what the top few qualifiers get. Adult females go through the same process, but since males produce up to ten times as many offspring a year, they are the ones most studied at the show by breeders and potential puppy buyers. The dogs that completely fail to engage, stay on the sleeve, and act protective and brave are sent home or to the kennel box — hopefully in the shade.

Now, here’s the rub. The judge who decides which dogs get the VA and high-V placings (and therefore will contribute most to the Hochzuchtlinie gene pool) does not get to see the actual performance in the courage test. In fact, he doesn’t even get a report on how well or how marginally the Ausgeprägt dogs really did. Many do not deserve a pronounced rating, although the 2006 courage test judge for males did a tougher, better job than average. So, how can the breed judge know what the character, as tested in the qualifying ring, is really like? He cannot. About the only thing he can use as a tiny part of his judgment, is the knowledge of whether the dog passed in the previous year.

In 2006, the Sieger was a dog that had failed the courage test at a prior BSZS, and at least half of his adult offspring did very unconvincing jobs in their own bitework. The vice-sieger was this dog’s father, who has not proven to be much better in either his own work or in producing brave dogs. Von Stephanitz must be turning over in his grave! In third place, a dog that perhaps should take their place next year, unless the Chinese snap him up as they are doing with so many dogs, is Orbit Huhnegrab. He, himself, did a good job on Friday, but had not a single offspring entered that was over two years old. A progeny class of untested dogs, no matter how good they look in stance or gait, should not be used to make a dog the Sieger. In the next several dogs in the VA group, problems with hip ratings, bitework, and other less-than-exciting qualities, made me yearn for the method used in the years of 1938, `41, `42, `74, `75, `76, and `77, when there was no Sieger named and the VA dogs were not ranked in order. I was so disappointed with the “Friday fiasco” lack of courage and preparation, and poor proof of progeny in the 2006 show, that I would not have awarded any VA’s at all.

I had a dream about a week after the 2006 BSZS, in which I was the judge doing the adult males conformation. Not only did I have the authority, but I also was in charge of organizing the show, and formulating official SV policy. I scheduled the courage test for males to begin on Thursday, and instructed the Leistungsrichter (courage test judge) to be as tough and demanding as he would be if he were doing it at the BSP. Instead of sequestering myself in a distant ring and only trying to see which dogs were prettier than which, I took private notes from my viewpoint, which was standing right next to the Leistungsrichter.

Later that night, he and I reviewed those notes and watched the video clips of those dogs that were in the running based on their show placings in previous months and years. We also looked at the films of dogs not usually shown — the “working lines” dogs, many of whom were hoping to compete for the Universal Sieger award, which is heavily weighted on BSP and other trial scores, but influenced by how high a V rating they get in the beauty shows.

In my nocturnal fantasy, I had the backing and encouragement of the Leistungsrichter when I moved certain great-working dogs up in the standings from where they would otherwise be if evaluated only on anatomy. Since the judges in charge of the adult bitch tests and show were in the meeting, too, I persuaded them to look at the bitches in the same light. Having seen several of the females work, I helped formulate those eventual placings, too. I decided to input data on Zuchtwert and “a”-stamp grades into the “calculations” — on a subjective basis, not a mathematical point system. The SV “a”-stamp has improved hip quality in the breed only up to a certain low plateau, and there must now be greater restrictions on what sort of hips and elbows we judges promote with our show placings.

As Chief Breed Warden, I was also formulating suggestions to improve the Zuchtwert system by including PennHIP data. This is the system, now widely used in Denmark, and increasingly in Belgium and Holland, that gives much better diagnosis because of much greater accuracy in determining joint laxity, and a better handle on heritability and progeny prediction. I also directed the responsible parties to work out an arrangement whereby non-German registered dogs could have their radiographs and allied data put into the SV system and database, so that “foreign” dogs did not have to start with 100 for their ZW value.

As an example of the present design not allowing sufficient information, the bitch from the Netherlands, Yasmin v. Nieuwlandshof, SchH3, (Erik Ehrenfeste ex Yelena di Fossombrone); linebreeding: 5-5 Enzo Burg Aliso) was outstanding in both anatomy and TSB. The ZW hip rating on this lovely granddaughter of Timo Berrekasten was 88, but it might have been even better had she not come from Holland and her dam from Italy. One of the bitches in my dream was “Space Geanie”, who in the real-life 2006 show got the only SG in the adult class, was instead advanced to a very respectable V rating in my dream. She gave one of the most exciting, positive, and pleasing performances of the day at Oberhausen. Excellence is more than croup angle and upper-arm length and layback.

Another that was very enthusiastic and practiced was Shalome vom Oasis, and I recommended to my fellow judge that he seriously consider her for Siegerin. Of course, outside of a dream, that would be looked upon as crude interference, but in my imagination-discourse, I was only doing what Captain Max would have done. Shalome had been consistent in both bitework and gaiting in the past as well as on this day. Other bitches that did well in both were VA 8 Oduscha Team Fiemereck, and of course Lothar Quoll’s beautiful VA1 Xara Agilolfinger.

My dreamland consultants and I returned to the subject of the males. They agreed with me that we should give much better placings than would otherwise be based on simply gait and stance, in such cases as the otherwise-V-132 Nando vom Haus Vortkamp. This male was breathtaking in his speed, precision, and enjoyment of being “macho-man” in the protection rôle.

The next day, when I had to build the preliminary order of highest-V down to the few SG dogs, I relied a great deal on the comments of my fellow judges, and the notes I took on the video review and during the protection work itself. The protection judge and my assistant who had done the statistical study were with me when I evaluated the structure, movement, and show history of the dogs in the past 18 months. All this was added to information on how many offspring had done poorly, how many were good, and how many were excellent in anatomy and/or work, especially in the previous day’s TSB. The percentage of progeny that passed the courage test, as well as the ratio of Ausgeprägt to Vorhanden, were part of the picture I based my rankings on.

After the decision on what placing each dog was given, all the Leistungsrichter (working trial judges) at the show came up and congratulated me on the primary emphasis I put on character. I reminded them that I was born the year von Stephanitz died, and ever since I became a show judge, I felt that I inherited his mantle, the way Elisha was chosen to continue the work of Elijah. I told the gathering that it was up to both groups to bring the German Shepherd Dog back to the center, where character, working ability, and usefulness to individuals and society are as important as such aesthetic qualities as good pigment, long croups, strong but normal toplines, good front angulation, proper dentition, and excellence in orthopedic matters.

But alas! Dreams soon are left to wither and fade on the pillow when the sun rises and pierces them with its burning rays. And the dream I was in, about being the Chief Zuchtrichter at the Sieger Show, was no exception. I woke to stark reality.

Instead of foreseeing the “total” German Shepherd Dog, it seems likely I will not live to see a single breed re-created from the two branches that now exist. It’s possible, but nothing to bet the farm on. As long as the breed judges (especially the ones choosing the top males) are isolated from even knowing how good or how marginal the TSB performances are, they will continue to choose on the basis of appearances (beauty) alone. They might as well stay home and judge from snapshots and video clips.

On the other hand, as long as BSP competitors and breeders ignore the cigar-shaped torso, the vertical front, the steep pelvis, and other problems, the gap will not be closed from their side, either. If breeders rely only on numbers — such as Schutzhund/IPO scores — they are also doing an injustice to the breed.

If show dogs need a SchH or IP or HGH title in order to gain recognition in the conformation ring, then “working-line dogs” should be required to have a V rating in the Zuchtschau or perhaps a Landesgruppe show, and a Körklasse-1a in order to rank in the top-ten BSP spots, or in the annual WUSV working trials.

The gap, the “great divide”, was not a creation or intention of von Stephanitz and his colleagues. Nor should it be continued by the SV and WUSV any longer. It was our (breeders, exhibitors, judges) creation, especially since the end of the 1960s, and we should be responsible for filling in that gap, for making the German Shepherd Dog one breed again.

Fred is an SV Zuchtrichter (Auslander), retired because of the mandatory age limit, but continues to judge in many other registries. He also presents seminars worldwide on GSD Structure, and on Canine Orthopedics. His articles can be found by putting his name in the Google or other search engines. He conducts annual non-profit sightseeing tours of Europe, centered on the Sieger Show (still the biggest breed show in the world). For tours or his books on Orthopedic Disorders or on the GSD, contact him at “All Things Canine” consulting division, Willow Wood Services: E-mail: