Canine Digestive Tract Disorders in Several Breeds (Part 1)

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:

  1. Megaesophagus
  2. Torsion/Bloat (Volvulus)
  3. Pancreatic Insufficiency (EPI)

Esophagus Affliction

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” ( 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” ( 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.]