Fred Lanting, © 2003
After skin problems, the next most common and next most frustrating set of disorders to the dog owner and the diagnostician are those of the alimentary canal, that tube through which passes food (and non-food, sometimes) from ingestion through defecation. It is said that the dermatologist has both the easiest and the hardest job: nobody calls him in the middle of the night or on holidays, but it frequently takes many months of trial-and-retrial before he comes up with the most likely diagnosis and then the cure is seldom totally effective. The internist also has a plethora of possible causes for digestive upsets, though not as many, and often he must likewise try several treatments before success. In addition, he is frequently called on for perceived emergencies.
The job of the digestive tract and the rest of the alimentary (food) canal is to take in nutrients, process the food for assimilation and conversion into body proteins, and expel what is left. Sounds easy, but many things can go wrong in that canal and in the organs that contribute to the digestive and absorption processes. These organs principally consist of the circulatory system, the gall bladder, and the pancreas. All add to or take away from the stream.
In 1990 I wrote an article entitled Digestive Tract Disorders. Having been requested to supply articles on bloat/torsion/volvulus, and on megaesophagus, I decided to combine some old pieces, revise the 1990 article, and work these into a new one with a new name. My favorite breed, the German Shepherd Dog, is susceptible to many gastrointestinal problems. There are a great number of causes for stomach and intestinal problems. When these two organs in the alimentary canal are considered together, we refer to a syndrome as gastro-intestinal. The three disorders I wish to treat here are:
- Torsion/Bloat (Volvulus)
- Pancreatic Insufficiency (EPI)
For no other reason than whim, let’s start at or near the beginning of this alimentary tract, where the esophagus meets the stomach. This is where a sphincter exists, that is supposed to keep the digesting stomach contents from refluxing back up the tube into the mouth (or worse, sidetracked into the lungs). Peristaltic action (a progressive squeezing, analogous to milking a cow, forces food boluses down from the mouth and throat to where they can be digested in the stomach and intestines.
Congenital pyloric stenosis is a similar disorder but is mostly found in Boxers and other short?faced breeds; it is very rare in the German Shepherd Dog. Spasm of the pyloric sphincter in excitable dogs, especially toys and miniatures, is also uncommon in the Shepherd Dog. There may be several other causes of esophageal dilation, affecting various breeds to different extents. However, German Shepherds have over thirteen times the incidence of esophageal disorders of all other breeds combined, although PRAA may be part of this statistic.
“Megaesophagus is the most common cause of regurgitation in dogs”, said Mary Labato, DVM, at Tufts University School of Veterinary Medicine. “It may be a primary disorder or secondary to esophageal obstruction or neuromuscular dysfunction. Among the causes: neuromuscular diseases, including myasthenia gravis, polymyositis (a muscle disease), polyneuropathy (affecting the peripheral nerves), dysautonomia (a rare disease involving the autonomic nervous system), systemic lupus erythematosus (an immune?mediated disease), polyradiculoneuritis (inflammation of the peripheral nerves and spinal ganglia), central nervous system disease, botulism, and damage to the bilateral vagal nerve that carries messages to and from the brain. Other causes include foreign body obstruction, stricture, neoplasia (various cancers), granuloma (inflammatory tissue), congenital vascular ring anomaly (vessel malformation), extramural esophageal constriction, hypothyroidism, hypoadrenocortcism, esophagitis, thymoma (tumor of the thymus gland), thallium (a metallic element), and lead toxins.”
Congenital megaesophagus occurs in young dogs and is a developmental abnormality of the esophagus. Megaesophagus-susceptible breeds include Irish Setters, German Shepherd Dogs, Golden Retrievers, Shar?Peis, Great Danes, Miniature Schnauzers, Wirehaired Fox Terriers, Newfoundlands, Pugs, and Greyhounds.
Frequently, large dogs are diagnosed with the idiopathic form in which the cause is unknown. Adult-onset megaesophagus occurs spontaneously in dogs 7 to 15 years of age. Dogs with secondary megaesophagus, as with myasthenia gravis, may go into remission and improve with appropriate treatment. “In most cases we don’t know the causes”, said Dr. David Twedt in the department of clinical sciences at the College of Veterinary Medicine and Biomedical Sciences at Colorado State University in Fort Collins. “Twenty-five percent of the cases have an underlying cause with the most common being myasthenia gravis.”
Congenital megaesophagus is also known by many other names such as cardiospasm, esophageal achalasia, dilated esophagus, and ectasia. The disorder appears to be caused by a simple autosomal recessive in German Shepherds, although it is highly variable in expression. After briefly consulting me, genetics worker Danielle LaGrave wrote an article for the November 2002 GSDCA Review on this subject, and concluded, “I had hoped to have a definitive answer as to how megaesophagus in the GSD is inherited. But regrettably, I was unable to.” My example of a pedigree study in “The Total German Shepherd Dog” (www.hoflin.com) apparently was not enough for her need to know the etiology, but is convincing enough to point to familial tendencies (heredity). While reportedly only about one percent of the dog population may be involved, mortality rate in pups is fairly high. Even when the far-less-common PRAA (Persistent Right Aortic Arch) has been ruled out as the cause, I believe the percentage of megaesophagus in German Shepherds is quite a bit higher than that reported one percent. Correspondents in the late 1990s have given me testimonial comments that they believe the incidence is on the rise, but this, too, may be more a matter of greater awareness. This abnormally large and flaccid “food-pipe” between the mouth and the stomach can be found in adults, but the most heartbreaking and serious cases are in pups early in the weaning and solid-food stage. The ballooning out reminds one of the extensibility of a pelican’s pouch. The more severe the expression, the earlier it manifests itself. There are two major types of megaesophagus; the early-onset, clearly hereditary kind with variable intensity, and the late-onset, acquired or secondary kind found almost exclusively in adults. Most of us have encountered many more cases of the former than the latter. Cases in young adults may not be easy to categorize as to type.
The worst cases starve to death by 8-9 weeks, others might have to be euthanized before 7-8 months. These represent the juvenile-onset, inherited type, not the adult-onset acquired type. GSDs, Goldens, and Irish Setters seem most at risk, and if a pup survives to adulthood, the condition often causes or is associated with other esophagus problems, peripheral neuropathies, gastric dilation with or without torsion, and especially myasthenia gravis. Even in adults, many are euthanized because of progressive malnutrition and owner frustration over the regurgitation. Or they asphyxiate due to aspiration pneumonia, vomitus obstructing the air passage. Most adult cases that are presumed to be acquired have no cause discovered, which leads us to believe some cases may simply be a milder form of the genetic problem that causes death by starvation in most pups between 5 and 9 weeks of age. Some veterinary references, however, stoutly consider these genetically- or environmentally different disorders. A loss of peristaltic action is probably due to a disorder of the afferent nerves. This is why there is no successful medical, pharmaceutical, or surgical treatment. There may be a connection with other nerve disorders, even giant axonal neuropathy, which mimics HD and GSD myelopathy. Some have gone so far as to hint that a general immune system deficiency is at the root of this problem, as it appears to be in so many disorders: pannus, Demodex susceptibility, DM, and more. I have elsewhere presented another article that treats this syndrome.
“On routine chest films, there is a large, usually air?filled esophagus, and frequently secondary aspiration pneumonia,” Dr. Twedt said. Symptoms of megaesophagus include slow or halted growth, weight loss, dehydration, water in the lungs, and persistent and progressively worse vomiting of food minutes after swallowing. The disorder usually is detected at or slightly after the commencement of weaning. As food slightly stretches the esophagus on the way down, an affected pup’s muscles apparently fail to contract enough to prevent the food bolus from staying in a pouch just in front of the entrance to the stomach. In time, the muscles become progressively weaker and less able to squeeze the food ball, and even liquid food remains in a hanging “pelican pouch” forward of and below the stomach entrance. As with PRAA, the pup becomes emaciated and listless, often dying of starvation. In fact, the two conditions may be indistinguishable without autopsy, but fortunately the incidence of PRAA seems to have decreased since the 1960s when I first encountered both disorders.
A definitive diagnosis can be obtained by giving a “barium swallow”, a concoction that contains heavy barium sulfate in emulsion or suspension, like a chalky milkshake. A radiograph is taken or fluoroscopy performed immediately after swallowing, and the opacity of the cocktail clearly shows where it is. Repeated views over the next several minutes will show the dilation and any obstructions to peristalsis. In the normal pup, the barium emulsion will be moving into and through the stomach, but in the dog with megaesophagus, most of it will be seen collected in that esophageal pouch ahead of the stomach. An experienced breeder or dog watcher may be able to save you a trip to the vet, but it is a good idea to make sure with a professional evaluation, so you can better plan the next breeding.
“Clinical signs of megaesophagus are regurgitation, wasting, and malnutrition, halitosis, hypersalivation, bulging esophagus at the neck, coughing, and increased respiratory effort due to pneumonia and muscle weakness”, Tufts’ Labato said. Diagnosis is confirmed by means of radiographs and other tests, which are intended to identify the underlying cause, and may include a complete blood count, chemistry profile, urinalysis, ACTH (adrenocorticotropic hormone) stimulation test, thyroid function test, acetylcholine receptor antibody titer to diagnose myasthenia gravis, and an antibody titer, which is a blood test that looks for immune-mediated disease in which the body attacks itself. Some perform the tests in conjunction with endoscopy, an electromyogram that measures changes in muscle tissue, and “bio-electrical” nerve conduction velocity studies.
Megaesophagus signs first appearing at old age are not typical, but dogs with “very mild cases” of the congenital type may not present with noticeable signs until older, when the owner perhaps is watching more, during and after meals. Also, similar symptoms can be caused by other disorders. One correspondent, when pressed on the issue of her 8 year-old “suddenly” showing signs, admitted that he had classic symptoms at 7-8 weeks (not long after weaning onto solid food), which points toward megaesophagus. A second opinion from a veterinarian who has a lot more experience in megaesophagus may have been needed, and that is what I advised her to get. I told her that there is a late-onset secondary form related to other disease states, but I was suspicious because of the history at age 7-8 weeks.
Mild or moderate expression of megaesophagus should not be a problem in the individual, non-breedable pet except after eating — which could be for many hours, though. If it is megaesophagus (inherited or acquired esophageal dilation) you might better control it by having the dog eat more-liquid-like meals, small servings, many times a day, and standing on his hind legs such as eating/drinking from a table with his front feet up where the bowl is. Also keep him as upright as you can for a while after meals. This might be the wisest management method. I suggested she might consult with a vet who would not advise surgery at this age — most surgical procedures to “correct” megaesophagus are not satisfactory. It is a very involved operation, with very low rates of success, and is highly expensive. Some dogs appear to outgrow the disorder, while others show no improvement, and owners must manage their feeding life?long. In a review of cases of dogs with megaesophagus with no identifiable cause, owners had 65 percent of them euthanized.
The height of the food bowl is a matter of controversy in the subject of torsion, and poorly-designed experiments have been inconclusive. But, for frank megaesophagus it is very helpful to have the dog in an “upright”, almost bipedal position, during feeding. There the bowl height is less important than the orientation of the esophagus. A vertical drop, small soft/liquid portions, and not feeding in the evening are good ideas. Feed small, wet/mushy portions throughout the morning and early afternoon, but not in the evening. A Tufts University bulletin in May, 2003 had a picture that illustrated feeding in a sitting-up position like that a dog uses when taught to “sit up and beg”. The owner of the case reported on for purposes of illustration made a special chair so the dog could eat in that position, which used gravity to help move food to the stomach. Keeping the dog in a vertical position for 15 minutes after each meal was most effective. The veterinarian told the owner to give wet dog food instead of dry, to feed him in a raised position, and prescribed medication to keep his food down, along with antibiotics. His total fee: $2,000. This owner learned that her dog did not benefit noticeably from medication; it even seemed to increase his regurgitating.
Following, in italics, is an excerpt from an article prepared by my young geneticist friend Danielle, for an American magazine. I have condensed it because of some parts being either obvious or redundant for an introduction. Remember that she is not a breeder, and did not have first-hand familiarity with the pedigree study I presented in my book, some generations of my own breeding a few decades ago. My comments are in brackets. “I am flattered that you want to include the article on the website. Please feel free to quote whatever parts you feel are applicable. Respectfully, Danielle.”
The answer to many questions depends on how “Mega” is inherited. There are two ways in which it might be inherited. The first is via an Autosomal Dominant (AD) gene. [Autosomal means that the trait is carried on some chromosome other than the X/Y sex-determining ones.] If the disease is AD, then only one parent needs to carry the mutated gene in order to have affected puppies, and would be affected itself. [Danielle says:] Approximately 50% of the pups in the litter should be affected, although that can vary from all to none based on chance. [Fred’s comment: this might be true only if the condition were a dominant trait with inhibited or partial penetrance, and I do not believe that to be the case, based on what I have seen; Danielle has not my breeding and observation experience, just the schooling.] Penetrance is the probability that a gene will have any phenotypic expression at all. When an individual with the appropriate genotype fails to express that genotype, you have a gene that shows “reduced penetrance”.
The second likely way Mega can be inherited is via an Autosomal Recessive (AR) gene. If the disease is AR, then both parents would have to be carriers (have one normal Mega gene and one mutated Mega gene). They would be phenotypically normal, and indistinguishable from a dog that does not carry the abnormal gene. However, when two carrier dogs are mated together, each pup they conceive, will have a 25% risk of inheriting the mutated gene from both parents, therefore having no normal version of the gene, and being affected. [Again, Fred’s comments: actually, 75% of the pups, on average, will inherit the defective gene; 50% of the offspring would be expected to be carriers and 25% would have a double dose and therefore clearly show the symptoms. The other 25% would be normal in both phenotype and genotype.]
So, if the disease is AD and the female has Mega herself then, yes, she can have affected pups even if the male does not carry the mutated gene. However, if the disease is inherited in an AR fashion, then both parents need to be carriers for the pups to be at risk. So she would not have affected offspring if the sire were not a carrier for the disease, even if she were a carrier. The problem here lies in that if she is a carrier, while she may not have affected puppies, on average 50% of her offspring [sired by a normal male] will also be carriers for the disease, perpetuating the abnormal gene in the GSD population. It takes both the sire and the dam to produce [overt] Megaesophagus in the litter if the disorder is inherited in an AR fashion.
At this time, there is no way to tell which pups are carriers. So you have a 2 out of 3 chance that the pup you choose to show and breed is a carrier for Megaesophagus. If you [in North America, anyway] breed the pup to another carrier (very likely if you line-breed) then your risk of having affected pups depends on the closeness of the relationship and whether the other dog has affected littermates or offspring (a fact you may never know). The math is simple. Let’s say you breed a bitch with affected littermates. Her risk to be a carrier is 2/3. You decide to breed her back to her paternal grandsire. His risk to be a carrier is ½ (Her sire must be carrier in this scenario (risk = 1) and he shares ½ of his genes with his father – ½ x 1 = ½ = granddad’s risk to be a carrier). This assumes that the grandsire has no affected littermates or offspring. So the chance for each pup produced by this mating to be affected is: bitch’s risk to be a carrier x dog’s risk to be a carrier x ¼ (each pup’s chance of being affected if both parents are carriers). In the above scenario this works out as follows: 2/3 x ½ x ¼ = 1/12. This is each puppy’s chance of being affected. The chance of at least one pup in the litter being affected would be higher, and would depend on the number of puppies.
[Danielle’s math is OK, but the statement that a show-pick pup from the bitch who had affected littermates had a carrier risk of 2 out of three is not a good way to express this. Make a Punnett square or other diagram and you will see that of four genotypes in her offspring (sire is normal, remember) one is homozygous-normal, one is homozygous-affected, and 2 are heterozygous-normal but carrying the recessive defect.]
If you outcrossed her, your risk to have affected pups would decrease, but since the carrier rate in the population is not known, the chance of having affected puppies cannot be calculated. Things get a little more convoluted when we address this question using the AD scenario. If Mega is a dominant disease it shows what is called “reduced penetrance”. Penetrance is the percentage of animals with the Mega genotype that demonstrate the Mega phenotype (are symptomatic). For example, in a [dominant] disorder with 75% penetrance, only 75% of the affected pups would be expected to show symptoms, so it is possible that an “unaffected” littermate is really affected but asymptomatic, and could still have affected pups. Therefore, the risk that one of the unaffected littermates could have affected puppies depends on the penetrance. The penetrance of the disease cannot be calculated until it is known that it is inherited in a dominant fashion. [Even then!] Dominant diseases often also show a trait called variable expressivity. What this means is that each dog which has the Mega genotype can express the phenotype to varying degrees. Some dogs may have the full-blown disorder with vomiting of solids and liquids and may need special assistance in eating (chairs to hold them upright, etc.). Others may only vomit solids and get by on soft diets. Some may grow out of the vomiting stage. And still others may barely be symptomatic at all and may never be diagnosed at all. These varying phenotypes may all be present in the same litter. So the pup that came to your attention due to vomiting and weight loss might have a brother who is gaining weight just fine, never vomits, and seems perfectly normal. However, if this pup had a [barium] swallow test at the vet, it would [might] be determined that this pup had Mega as well. So it is important when one pup in a litter is diagnosed with Mega, that a vet with knowledge and experience in diagnosing Megaesophagus examine all the pups. If you bred this “normal” pup, he would be expected to sire pups with Mega.
[Unfortunately, the same scene can be, and I believe definitely is, painted with the AR (recessive theory) brush. What we breeders have seen is that there are “modifier genes” located either close to or far from the major gene responsible for a recessive trait, on the same or different chromosomes. These account for such differences between littermates as amount of gray grizzling in the saddle, relative darkness of the iris, amount of hip joint laxity, etc. I believe such modifiers are most likely the primary cause of differences between affected (homozygous-recessive) littermates with megaesophagus. Further, the effect of environment cannot be ignored; I believe there is a substantial contribution to phenotype there. Some pups with a borderline condition, held in check for a while by those modifiers, could be pushed over the line into obvious pouch dilation by feeding techniques. Conversely, a pup with a mild form might grow up to have stronger muscles around the length of the esophagus, if it had been fed small frequent quantities of soft mush, while standing on its rear legs, and handled in other manners designed to prevent stretching of the esophageal tissues. Other pups will vary even if the same treatment is given to all.]
If the goal of the breeder is to eliminate this disease from their line (and ultimately from Germans Shepherd Dogs, entirely), then dogs that have affected offspring or have affected littermates should not be bred; we would greatly reduce the number of affected alleles in the breeding population. If the disease is [recessive], then it will take a while due to those pesky carriers that never had an affected litter [to tell us] they are carriers) until genetic testing is available that can detect carriers. If it is AD, it can be eliminated in a very few generations, even with reduced penetrance. [The condition is more common in the U.S. than hemophilia or epilepsy was in England just a couple decades ago, and since it has not noticeably diminished in linebred American-AKC type dogs, this is another strong hint that it is a recessive trait.]
If your goal as a breeder is to not eliminate the gene, but to only avoid affected pups, then it is necessary that you perform in-depth research into the lines of the males you choose for her. The same logic applies to stud dogs as to the bitches; the main difference is that some studs contribute their genes to a larger proportion of the next generation(s). If you feel that your bitch’s positive contributions to the breed far outweigh her negative contribution (the Megaesophagus gene), and you do decide to breed her, you need to determine that the potential sires have no offspring [or relatives] with the disease and have every puppy checked for Mega by a vet. If the disease is inherited in an AR fashion, then you are breeding a known carrier (having affected offspring is a very accurate test for carrier status!). Remember that ½ of her pups would be carriers and we can’t tell which. [Actually, your Punnett square will show half to be apparently normal but carriers, 25% will be overtly affected, and 25% genotypically normal. For more on the Punnett square visualization of inheritance modes, see my book, The Total GSD, and articles of mine on genetics found on various websites.]
If a very popular male is a carrier of Mega, he can have a devastating effect on the allele frequency in the population. His popularity can cause the number of carriers in the population to rise sharply. Then, as these dogs are bred (and often line bred) the number of affected pups jumps. A female has fewer chances to contribute her genes to the next generation. [This has happened. The pedigree study in “The Total German Shepherd Dog” (www.Hoflin.com) indicates that both Bernd Kallengarten and Lance of Fran-Jo were suspects in carrying the recessive for megaesophagus. The popularity of combining these lines for success in the show ring was mirrored by a large number of affected pups. Most died at or shortly after weaning age (5 to 9 weeks) despite attempts to save them. A good friend who had carriers and affected dogs had an attitude that was typical of many: he felt that the worst ones would self-cull by dying, and those that survived would be as acceptable for breeding as their show-successful parents.]
In the AR scenario, a dog with a genotype of mm [homozygous and affected, even if not obvious], can only contribute mutated genes. 100% of [its] offspring will at least be carriers of the disease. Some percentage will be affected as well, depending on the carrier status of the other parent. In the AD scenario, each pup will have a 50% risk of being affected. Even the ones that do not show signs of disease may have affected offspring due to reduced penetrance. [I disagree, and feel these last two sentences are potentially confusing; in my experience, 100% of the pups in a litter with one dominant-gene parent (or both) will be affected. Modifier genes can indeed cause phenotype variability. But it is less than academic, since I am quite sure that megaesophagus is recessive. Besides the litters I’ve seen, other weight is given by the fact that most disorders are recessive in essence. Nature tends to weed out defects through the laws of natural selection and “survival of the fittest”. It is man that has created, by protective and selective measures, such defects as are now accepted as “desirable”, such as pushed-in faces, dwarfed legs, extreme size, and other anatomical and behavioral features. Likewise, by benign neglect, man has also interfered with Nature’s tendency to keep defects at their lowest incidences.]
Never breed an affected dog; even an affected dog who “has recovered” should be neutered and all littermates tested. If the goal is to eliminate the disease, then any carrier risk should not be bred. Of course, this applies to the parents as well. They are “obligate carriers”, and will continue to contribute the gene to their offspring even if they never have another affected puppy. One source states that the incidence of Mega-esophagus in the GSD population in the US is approximately 1%, although the author [LaGrave] speculates that it may even be higher. If 1%, then about 18% of US German Shepherd Dogs are carriers of the altered gene (assuming AR inheritance). With 18%, the [risk], even if you avoid line breeding and stay completely away from all the [known] lines is extremely high. [Fred adds: I do not see the occurrence of megaesophagus in other countries where I have judged, as being anywhere near the magnitude as it has been and probably still is in the U.S. The reason? Bloodlines, probably. After the mid-1960s, the lines diverged tremendously from those in the rest of the world, those being primarily in close alignment with current German genes. Some were isolated by government quarantine and that included the “Alsatian” in the U.K., and the lines in Australasia. The relative isolation in North America was one of breeders’ choice and fad preferences as much as it was the control by a powerful political clique.]
Breeders’ responses to early puppy deaths vary. Some expend a great deal of effort, while others “let nature take its course” and stoically hope the next breeding will be more successful. Many have discovered that neonatal puppy mortality is preventable or call be reduced through scrupulous attention to prenatal and postnatal care. These breeders, who in the past may have accepted 20 to 25 percent mortality before weaning, have learned that such losses can be reduced dramatically by simple changes in management, including veterinary checkups. Continue reading
To all who are interested in the 2009 Sieger Show in Germany. Also, a request to website owners to make it known on your pages:
Please let your “doggie” friends know that time is getting short, in regard to plans for this year’s (non-profit) Sieger Show trip. In order to make sure of rooms and rental vehicles, I need definite commitments (deposits and details) from all who will participate. Please forward to any and all who you think might be interested in joining this year’s show and tour. Thanks. As always, I divide my expenses-only among the participants.
We will arrive in Munich the morning of August 27 (Thursday), which will mean those coming from the USA or some other countries must leave at least the previous day. Kennels are relatively scarce in Bavaria, but I have arranged a visit to the famous WildsteigerLand and am waiting for confirmation re the Jahnhohe folks. Unfortunately, very few clubs have training functions during the week following the big show. Also, the number of tour participants who have signed up so far is so low, and the US economy such that I had to shorten it by one day compared to previous years’ length and activities.
You will meet breeders, get an SV judge’s perspective on the show and dogs, have your questions answered, and enjoy one of the most delightful parts of Germany. Including some fantastic scenery, the castles of King Ludwig (one of them inspired the Disneyland “castle”), the Alps, Bavarian costumes & food, and more. Most flights leave Munich early-morning on Wed., the 2nd of Sept.
Again, I urge you to forward this to anyone possibly interested, and to websites that might reach those who do not know about the tours I’ve been leading for the past two decades. Join us and Gemütlichkeit! Fred Lanting, tour guide
© 2006 by Fred Lanting
[Note: the original appearance of this article did not include “and Other Breeds” in its title, but since then I’ve had many reports of dogs of different breeds being similarly affected, with demodex and thyroid insufficiency at the top of the complaint list.]
The German Shepherd Dog is a very popular breed. In fact, it is Number One worldwide although in the U.S. it ranks much lower partly because of AKC clubs’ non-adherence to the international Standards — usually in the AKC top ten, though. As a result of there being so many GSDs, veterinarians and others typically see more cases of most disorders than they do in other breeds. Popularity has its drawbacks, and undeserved notoriety is one of them. Take the incidence of dog bites, for example. Many breeds have far more of a tendency to bite people than does the GSD, although they don’t get the same “press” (publicity). Min-Pins, Skye Terriers, American Cockers, Chows, and many others will sink their fangs in you more readily and with less provocation. But the popularity of Shepherds, Rottweilers, and a couple others is their downfall.
Of course, not all popular breeds are involved in as many biting incidents. You have to travel a long road to find a Golden Retriever that has ever bitten a person, and Labs have an intermediate incidence compared to others of its size. Nor do big dogs bite more (although perhaps with more damage) — the mastino types are usually placid, while the feists like Chihuahua/terrier-types and mixes give credence to their name and the word “feisty”.
That was just an example of generalizations that abound in the dog world. Some are unfounded; others have a basis in statistical facts. Another example is the incidence of hip dysplasia. Rottweilers and American Pit-Bull Terriers may have nearly the same percentage and typical severity of HD as in the GSD, but the Shepherd is almost unique among breeds in that HD causes more discomfort and lameness than same degree of looseness in the joints of the more stoic breeds with some bulldog heritage.
Another problem seen quite frequently in the GSD is the deficient immune system syndrome (a syndrome is a collection of symptoms). It is characteristic of this problem to manifest itself in one dog in a certain way, and in another dog in a different way, a little like a pleiotropic trait. Some evidences are so slight that many owners and vets miss or don’t guess at the underlying cause. This leads the doctor to wrongly prescribe a certain medicine or none at all, and the breeder to go ahead and breed a covertly defective dog that should not be mated. Further complicating the matter, and preventing as much progress as could be had, is the subclinical nature (a lack of, or hardly-noticeable, signs. Many intermittent or mild complaints that owners have are not identified as related to the dog’s immune system, and others have taken years of badgering by breeders before the veterinary community has acknowledged what breeders had known all along. So you will find some disagreement in some of what I will present in the following material. I don’t want to just list a table of disorders under the subject heading, but you might want to do that for yourself. Let’s take a look at some of those immune-mediated disorders after a few more words about the general subject.
The GSD has more than its “fair share” of immune-related problems, and they appear in the intestines, eyes, skin, and other places. The breed has many individuals with a deficiency of a particular immunoglobulin called IgA, and this genetic defect may be very close on the chromosome to genes controlling general immune problems.
The dog’s “Defense Department” has a number of soldiers: antibodies, immunoglobulins, specialized cells, and more. Some vaccine ingredients, adjuvants, or carriers have been known to cause an over-reaction by this army and result in an autoimmune situation in which the body also attacks its own cells. A recent vaccination development called “recombinant vaccine”, helps avoid bad reactions to vaccines or the medium in which they are cultured or carried into the blood system, but is not effective against parvo. Nowadays, the over-reaction is more often a matter of genetics than any stimulus from vaccine components.
The German Shepherd Dog is at risk for a number of immune system abnormalities, and while not all have been directly linked to immune suppression, there is great suspicion of a connection with most of them. We have seen such problems in the breed as pannus (chronic superficial keratitis), corneal dystrophies, and plasmacytic conjunctivitis in the eye; lupus and anal furunculosis in the outer integument; and plasmacytic colitis in the gastrointestinal tract; these we suspect are related to autoimmunity. The various components and functions of many glands and chemicals in the normal body are lumped together to refer to their joint action of protection, and given the name “immune response” or “immune system”. It involves such things as T cells, phagocytes, white blood cells, antibodies (immunoglobulins), complement proteins, and others. Together, their job is that of a second line of defense against antigens and other threatening “foreigners”; the skin, mucous membranes, and stomach acid are some of the first-line defense mechanisms that bodies have, and if something harmful gets past the frontline troops, the interior guard must go to work.
Invading organisms may be viral, bacterial, parasitic, fungal, and may come into the body via puncture, swallowed foreign objects, impurities in eaten material, absorption through the skin, intake by the lungs, or other routes. This second line of defense even goes after waste generated in the cells, or abnormal cells which if left alone could become cancerous. To do this, the soldiers must be able to recognize the enemy, and do so by chemical means, such as “seeing” if the projections on the suspects fit like jigsaw pieces into receptors carried by the troops. If so, they attempt to neutralize by putting chemical handcuffs or a half-nelson on those invaders until they can dispose of them. Some of the home guard, macrophages, actually “eat” bacteria; some poke holes in the invaders or mark them for other cells to eat or destroy. When such interactions occur, the guard is stimulated to call for reinforcements (multiply rapidly) to search for more of the invaders’ ilk. Our B-lymphocytes have antibody protein molecules on their cell surfaces that recognize the foreign molecule called an antigen. One result of this encounter is that these B “white blood cells” become antibody factories called plasma cells, and can turn out their product for many years to come. Thus, some diseases are warded off the rest of our lives because our bodies continue to have patrolling soldiers that can recognize them. The other type of defender lymphocyte is the T cell. They directly kill “bad” cells without using antibodies. Besides killer T cells there are helper T cells and suppressor T cells; the latter call off the attack so the white blood cells (lymphocytes) don’t get carried away over-multiplying (hopefully!) or that would present other problems.
One hitch in the war machinery is that some lymphocytes get confused and mistake normal body (called “self”) proteins for the “bad guys”. If “Self” doesn’t kill off these errant traitors, as normally happens in the embryo and very young individual, we have what is called an “autoimmune” situation. An oversimplification would be to say that the body is “allergic to itself”. In any case, the body uses the home guard to attack and possibly destroy part of itself (its self). Such a defect can affect immune response all through the body. It is possible that this is happening in pannus, “allergies”, lick granuloma, and a number of other problems in your or my dog. In human AIDS, all the active helper T cells are destroyed, so the body no longer has adequate defenses against any and all antigens. In most disorders, only one or two pathways are affected, so a problem may show up as an itch, skin blisters, hemolytic anemia, a corneal defect, rheumatoid arthritis, or something else in one or more organs.
Demodex — One of the most easily identified immune-mediated problems is demodectic mange. To distinguish between this and the purely contagious sarcoptic mange, see some of my other articles or buy my book on the GSD. The demodex mite is ever-present on nearly all dogs and humans, but doesn’t cause a problem unless the host is weakened by something, especially another immune system related disease or stress. It is widely believed that stress of various kinds, whether of a genetic origin such as a very nervous temperament, or either a genetic or acquired immunodeficiency disease that suppresses T?cell function in the immune defense system, may be the major factor in an outbreak of symptoms such as demodecosis in a dog. With lowered cell?mediated immunity, the individual reacts adversely not only to the mite and its toxins, but also to the presence of other microbes and antigens. “Neutering” reduces stress in the individual and helps brake the spread in the gene pool. A bitch in estrus is in the highest state of systemic stress that any dog normally encounters, outside of severe trauma and shock. Often enough, demodecosis is concurrent with another immune-related defect. If your dog has demodectic mange, look for another condition that should be treated at the same time. Is there a history of subclinical pancreatitis? Has there been recent surgery or other physical or emotional trauma? Any exposure to debilitating diseases? Even the minor stress of teething may be sufficient to tip the balance and encourage sudden proliferation of mites and their symptoms in susceptible dogs “on the borderline”. Very healthy dogs rarely show symptoms even when exposed intentionally by clinical transmission of the mites. Stress (such as illness) seems to “awaken” the mites. Combating demodecosis is largely a matter of curing or controlling the dog’s other ills, both physical and psychological. Use of steroids is contraindicated because they compromise the dog’s immune defense. See my “Total German Shepherd Dog” book for more detail on this topic.
Pancreatitis: In its chronic, subclinical, or often-undiagnosed mode, exocrine pancreatic insufficiency (EPI or PI) is fairly common in German Shepherd Dogs of certain bloodlines. It has even been identified with demodectic mange, possibly because during the stress of the dog’s affected digestion, its body is less able to immunologically suppress the proliferation of the mange mites. Supplementation with vitamin A and pancreatic enzymes should be supervised by a veterinarian who is knowledgeable in this area and has been made aware of the genetic nature of the problem in certain lines of our breed. The occurrence in pancreatic insufficiency among German-line dogs in the U.S. has increased since the 1970s, but I believe there are a couple of different reasons for this, if it is an accurate observation.
Malabsorption (poor digestion and poor stool condition) are frequently seen in the GSD, and in my experience, has been more so in the heavily linebred typical lines in American-bred dogs since the 1970s. EPI is one of the conditions that can contribute to the malabsorption syndrome. The symptoms can be exacerbated by physical or emotional stress, change of food, and other things. I suspect that dogs with subclinical weakness in immune systems or pancreatic function may be most likely to show these reactions. With EPI, the fur often becomes dry and brittle, and even lost to some extent, and Staphylococcus infection scabs may appear on the skin because the compromised immune system doesn’t allow the dog to fight off the infection. The symptoms of EPI mostly show up when the TLi value is down (Trypsin?like immunoreactivity test). So there seems to be a possible connection, with insufficient pancreatic function and other resistance” all being tied to the immune system.
A dog with the sub-acute form of pancreatitis may exhibit coprophagy, which means he eats his own (or others’) stools. It may be that he smells the undigested fats and carbohydrates and instinctively consumes it as food to give those nutrients “another chance.” Often, the addition of liver to a low?fat diet and daily administration of enzyme powder or capsules, or regular supplementation with ground pancreas if you are lucky enough to get some from a nearby slaughterhouse, will bring the condition under control or at least improve it. Researchers at Tulane University found that a commercially available enzyme supplement could improve blood analysis, neonatal vitality, digestion, and general health. The manufacturers of Viokase™, a dried raw pancreatic enzyme brand, have shown that supplement/medicine to be effective in combating nonspecific diarrhea as well as German Shepherd Dog subclinical pancreatitis. The juvenile-onset generalized demodecosis often has a spontaneous semi-remission because of better stress management.
Dogs that exhibit symptoms such as much flatulence, or intermittent diarrhea or pasty light-brown/yellow to clay-colored stool, perhaps should be tested for levels of Lipase, Protease and Amylase, or just fed the recommended preparations without testing. But keep an eye out for other immune-system signs, too. Some people perceive a probable connection or coincidence between anal furunculosis (perianal fistulas) and EPI. Both of these problems may show up in the same dog, strengthening the suspicion that they are manifestations of the same underlying immune system weakness. A great deal of the digestive tract functions and stages may be affected one way or another by the same genes governing immune response.
Pancreatic insufficiency is an abnormality that suggests removal from the gene pool, whether the dog has a severe or a mild case or is asymptomatic most of the time. Most vets take very few hours of nutrition and practical genetics classes in vet school, and then forget most of it because they don’t use it every day. Breeders are sometimes more reliable sources of information. Unfortunately, many people who offer their EPI males at stud do not admit or declare any cautions about their dogs. As one observer quipped, “It’s funny isn’t it, that those who deny all those things have Viokase-V on the shelf in their back rooms?” Although it is good for various unspecified causes of diarrhea, the product is so much more expensive than Kaopectate, that it makes you wonder.
Bloat/Torsion/Volvulus: Is there a connection between PI and GDV (gastric dilation and volvulus)? There have been reports from dog owners indicating that many episodes of EPI begin with a bloating incident, or with a gastroenteritis, marked by vomiting and blood tinged diarrhea. One observer said, “From the general info collected, the dog first bloats, which often leads to torsion of the gut, which of course requires surgery for a tacking of the stomach, and this is usually followed by a full blown episode of EPI within a few months of the surgery.” I suspect that there is, at least sometimes, a common root cause if these two problems. Dogs with a history of bloating/torsion and/or bouts of unexplained diarrhea are reported by several of my correspondents to be quite likely to be EPI-carrier suspects, although this observation is admittedly anecdotal.
Megaesophagus: German Shepherds have over thirteen times the incidence of esophageal disorders of all other breeds combined, although PRAA, an unrelated heart defect that causes similar symptoms as caused may be part of this statistic. Dr. Labato at Tufts U. School of Veterinary Medicine says, “It [sometimes] may be secondary to … myasthenia gravis, systemic lupus erythematosus (SLE is an immune?mediated disease), …[and possibly others].” Breeds susceptible to the juvenile-onset, inherited type of megaesophagus include Irish Setters, German Shepherd Dogs, and a few others. Frequently, large dogs are diagnosed with the idiopathic form, which means the cause is unknown. “In most cases we don’t know the causes”, said Dr. Twedt in the vet school at Colorado State University.
The characteristic loss of peristaltic action is probably due to a disorder of the afferent nerves, which is why there is no successful medical, pharmaceutical, or surgical treatment. There may be a connection with other nerve disorders, even giant axonal neuropathy, which mimics HD and GSD myelopathy. Because of these similarities, some have hinted that a general immune system deficiency is at the root of this problem, as it appears to be in so many disorders.
Diagnosis of megaesophagus is confirmed by means of various tests, some of which are intended to discover the underlying cause, and may include the acetylcholine receptor antibody titer that is used to diagnose myasthenia gravis. An antibody titer is a blood test that looks for immune-mediated disease — one in which the body attacks itself. One source I detail in my GSD book states that the incidence of symptomatic mega-esophagus in the GSD population in the US is at least 1%, but about 18% of U.S. (AKC-lines) GSDs are carriers of the altered gene (assuming autosomal-recessive inheritance). With 18%, the [risk], even if you avoid linebreeding and stay completely away from all the [known] lines, is extremely high. The pedigree study in “The Total German Shepherd Dog” (www.Hoflin.com) indicates that both Bernd Kallengarten and Lance of Fran-Jo were suspects in carrying the recessive for megaesophagus, and the latter was known to produce a considerable number of descendants with various other manifestations of immune defects.
Intussusception: In very young pups (and other animals including humans) the intestine can invaginate (one part slips inside another). The condition, also referred to as “telescoping intestines”, also occurs in adults, but not as frequently. Most common immediate causes include worms, obstruction by indigestible materials, garbage, or toxic substances. However, since the German Shepherd Dog seems to experience a relatively high incidence of this disorder, I have to suspect the possibility that (other than those above causes) there is a genetic propensity in certain bloodlines, and perhaps interrelated to other “GSD disorders” — those more common to this breed than most others.
Pannus: The GSD has more than its “fair share” of immune-related problems, and they appear in the intestines, eyes, skin, and other places. The breed has many individuals with a deficiency of a particular immunoglobulin called IgA, and this genetic defect may be very close on the chromosome to genes controlling general immune problems. The GSD, after the West Highland White Terrier, probably also presents most of the cases of pannus, an eye disorder caused by lymphocytes migrating into the cornea and causing blindness unless treated. More and more vets are referring to it as chronic superficial keratitis; CSK for those addicted to abbreviations. I have watched quite a few eyeballs “peeled” in the surgical part of the therapy, in the days when steroid drops in the eye on a frequent basis (several times a day) for the rest of the dog’s life was the post-surgical treatment of choice. Peeling was the more heroic procedure, when injection of cortisone under the conjunctiva as a first step is not effective. Today the drug cyclosporine is used to best advantage in pannus, although a steroid such as dexamethasone is still effective. This cyclosporine is the same drug, originally found as a component of a Norwegian soil fungus, that is given to counteract the body’s tendency to reject other people’s organ transplants. The drug is given as an ointment or in food twice a day until the cornea is free of the lymphocytes, then there is a once-daily administration; it seems to work partly by causing the tear ducts to operate almost full time. Enough is absorbed by the tissues of the eye to get into the far reaches of the circulatory system where it does the other part of its job, fighting those wayward lymphocytes.
No cure is in sight, since it is highly likely that pannus is an inherited autoimmune disorder, and people who have dogs with pannus will have to deal with the frustration and regimentation of daily treatment for the dog’s lifetime. The same situation has been nagging sufferers from human autoimmune disorders for a long time. MS, multiple sclerosis, is considered by most to be such a disease, in which T-cells attack components of the central nervous system (brain, spinal cord and some major nerves). One of those components, myelin basic protein (MBP) has been experimentally fed to lab animals, and later to human MS patients, and it was discovered that the severity of symptoms was considerably reduced. Rheumatoid arthritis, dealt with more in my book on orthopedic disorders, is another supposed autoimmune pathology in which the T-cells act against parts of the joints, especially Type-II collagen. Again, oral-dietary administration of this type of collagen was fed to RA patients with significant improvement in managing the disease symptoms such as number and severity of swollen joints, gripping strength in the hands, and subjective descriptions of pain or stiffness after rest or sleep. Experimental treatments involving feeding normal cornea extracts to dogs with pannus may have similar results.
Pannus was previously called “keratitis superficialis vasculosa pannosa pigmentosa chronica”, “German Shepherd Dog Keratitis”, and “Keratitis Überreiter” after its Austrian discoverer, is an inflammation and pigmentation of the cornea and sometimes involves the conjunctiva. It is rare in almost every other breed, and in the GSD it usually appears around 3-5 years of age and in both eyes. By that time, many affected dogs will have already been bred. Besides the hereditary, breed-dependent predisposition there is an environmental component that brings it on earlier and more certainly: ultraviolet radiation. UV rays in sunlight trigger the onset of symptoms, explaining why an increased incidence is observed anywhere during the sunnier months of the year, and more cases are presented in higher elevations such as Denver. This means that to avoid outbreaks of the acute phase, the owner should not only keep up with the medication schedule, but also make sure his dog is protected from exposure to strong sunlight, even if reflected off snow or water, and especially at high altitudes. Some dogs are kept indoors (glass windows filter out most UV rays) and are walked in darker hours; some wear fitted sunglasses.
Corneal dystrophy: While I do not draw any definite connecting lines between pannus and this disorder, I mention it because I think there may be an immune system relationship. Small opacities may appear on the cornea over the pupil or slightly off-center, and the novice might think the dog has cataracts. It may be triggered by an allergic reaction or some other cause, and show up as a small spot, varying from slightly translucent to cloudy-white. The size is usually less than 5mm across, round, oval, or horseshoe-shaped. Most eye specialists refer to this type of opacity as “corneal dystrophy”; the spots do not interfere with vision. In my experience the spots have faded away in a few years after reaching maximum size. Corneal dystrophy appears to be genetic, but is not serious. Probably less than one percent of the breed is affected. I once had a bitch who developed very small oval opacities, one on each cornea, after she was about four or five years old. They finally and gradually disappeared (shrunk to nothingness) by the time she was about ten years or more. This bitch also developed atopic (allergic-type) problems marked by itching feet and sometimes parts of the skin, but most noticeably by an assumed feeling of excess phlegm in the throat. One of her many sons developed the same transient and minor corneal defects, appearing in maturity and going away without treatment by old age. While it is possible that some of these opacities may be immune system related, I think most are largely if not fully environmental.
Pemphigus: Uncommonly seen in dogs and more found in humans, this group of related autoimmune disorders involves mostly the mucous membranes and skin. You may never notice the spider-web mucosal condition in the mouth or purplish, fragile splotches of skin in some forms. In some forms it can produce ulcers in mucous membranes. Very high doses of corticosteroids for life may control the disease, but this is a controversial approach because steroids are generally contraindicated in autoimmune diseases, and usually cause a great deal of capillary rupture and bleeding. It may be best to just leave these alone and see if they will “go away” on their own.
Primary Seborrhea: I have no hard evidence, but I suspect seborrhea may sometimes be a sign of an acquired autoimmune disorder. This disorder is a condition in which there are scaly patches and a greasy feel to parts of the dog’s skin. You will probably notice great difficulty in keeping the ears clean and free of dark wax and yeast or fungus. Often, the older, long-affected dog will have an over-all rancid odor. Many of these cases are related to thyroid hormone imbalance, and such an immune- and general endocrine-related disturbance may become chronic and in need of very frequent bathing and/or ear cleaning with little or no hope of remission.
I have seen many cases that have been brought on after extended or repeated exposure to fleas and other factors. The flea allergy or exposure may be the prime cause of the skin condition, with the flea antigens weakening the dog’s immune response and thyroid function, resulting in severe seborrhea. Or, the immune defense weakness may be the prime cause of the dog not being able to withstand fleas. Ask a veterinary dermatologist to try to find the underlying cause as well as give you ideas on how to treat for the symptoms. If the dog shows evidence of much itching, it is usually called secondary seborrhea, which refers to a primary cause being mange, fleabite allergy, or other trigger influences, involves relatively large reddish-skin patches with hair loss, and is often more scaly and less greasy than is the primary form. Primary seborrhea is something GSDs seem to be more predisposed to than are most other breeds, and it is this type that more affects the ear with fungus growth, and sometimes an increase in bacterial colonies on the skin. It is a chronic condition that requires constant or renewed treatment regimens with no hope of eventual cure, just some control.
Most owners of dogs so affected report considerable success in managing or partially suppressing the symptoms by attacking them on several fronts: get rid of fleas (and the cats and carpets they rode in on!), clean the ears daily or several times a week with a 50/50 mix of vinegar and water, and temporary regimens of Soloxine (thyroxine) for perhaps two weeks at a time. Your vet can suggest a dosage level to try, of this quite safe internal medication.
Degenerative Myelopathy: DM was once as “GSD myelopathy” because most cases in the early days of investigation involved this breed. It is the first disorder that comes to mind when German Shepherd Dogs and spinal lesions are spoken of together. “Degenerative” means that it is chronic and progressive, and “Myelopathy” means spinal cord disease. The first symptoms are usually seen at about six to eight years of age and have a duration of five to twenty-four months, perhaps a bit longer if aggressive measures are taken, but who knows if they are really effective? Initially, the dog does not seem to realize what position his rear legs are in; soon he will begin to drag his toenails and the top part of his paws, and later may tremble as if palsied. Eventually, he will be unable to get up on all four legs, and by this time most owners will have decided upon euthanasia. Symptoms and histological changes are very similar to those in multiple sclerosis (MS).
It is also seen (though rarely) in the Belgian Shepherd and the Old English Sheepdog, and some authorities feel that other breeds’ degenerative myelopathies are probably not caused by the same immune-system deficiency as we have in the GSD. Autopsy shows demyelination (loss of the insulating sheath) of the spinal cord, destruction of some large axons (nerve cells leading from the cord to smaller branch nerves), and abnormal cells (or certain cells in abnormal locations). Similar signs may be seen in the brain, kidneys, and intestines, giving further hints of the immune system failure being at the root of this disease.
It may be that relatively high vitamin E dosages may be helpful, but it is difficult to compare a particular dog’s disease progression with a “what-if” situation. We have a good idea that this vitamin is very helpful in immune response improvement, so it is natural to assume a probable direct benefit in this immune-related disease. 800 units (IU) a day may be enough, although some years ago one researcher claimed that 2000 IU of vitamin E daily, 500 mg of vitamin C twice a day, and a high-strength vitamin B complex twice a day was the best dosage. In DM dogs, low serum and tissue concentrations of vitamin E have been observed. I recommend that vitamin E be given to all older German Shepherd Dogs for general resistance and health. It can’t hurt — they will excrete anything they don’t need, within reason. Chemical-pharmacological treatment has largely been via the use of aminocaproic acid, and more recently, acetylcysteine three times a day found acceptance, although conventional drug therapy (medicines) has been of little lasting help to patients with DM. The combination of exercise, vitamins and certain drugs seem to have delayed the progression of DM in many dogs. Treatment has been directed at suppression of symptoms and the multi-pronged approach may prolong the day you have to face euthanasia because of debilitation and inability to stand to defecate or to walk.
Lick Granulomas: Dogs with GSD myelopathy often develop lick granulomas on hind feet, which are non-healing ulcerations or (if you are lucky) callous-like reactions of the skin to extremely frequent licking, sometimes chewing, at the location of a supposed itch. It is probably a case of the limb feeling as if it has “fallen asleep”, to put it into terms familiar to human experience. The tingling sensation caused by incomplete and erroneous signals by the nerves serving that place is much like the irritation caused by an ant bite, or hairs out of place, or anything in between. In trying to lick it away, the dog actually softens and wears away the hair and skin. Lick granulomas are not restricted to dogs with DM, but often occur on the pasterns or toes in dogs that have atopic allergies, another clue to the presence of a general immune system deficiency.
Other problems: Keep in mind that the various parts and systems of the body are all inter-related, that a disruption in the process of one may have an origin or an effect in another. The endocrine system is a prime example, with hormones being produced in more than one gland and greatly influencing some or all of the other glands. Something that has not yet been thoroughly explored in veterinary schools or with research grants is the collection and inter-relation of problems very common to GSDs, with yeast/fungal infections, flea saliva allergens, and general autoimmune system weakness. I have observed countless cases of dogs in this breed with a combination of seborrhea, low resistance to fleas, thyroid insufficiency, nagging ear infections, interdigital pyoderma, and other “complaints”. The lines between these dots, I hope, will someday be drawn with more clarity.
[Author Fred Lanting <email@example.com> is an international show judge for many registries, presents seminars and consults worldwide on such topics as Structure, Orthopedic Disorders, Training Techniques, and the GSD. Fred invites all to join his annual non-profit Sieger Show and sightseeing tour. He actively trains in Schutzhund, and breeds occasional litters of GSDs (see his dogs on http://www.angelfire.com/de3/jagenstadt/vonsalixHome.html ). Most articles can also be found on http://www.fredlanting.org or others by a Google search for his name. Reprint permission of these copyright pieces can be requested and should carry this or a similar notice at the end.]
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
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
“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
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
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.
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: firstname.lastname@example.org
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