Having been requested to supply articles on bloat/torsion/volvulus, and on megaesophagus, I decided to revise an article formerly published as “Digestive Tract Disorders”, and combine it with other articles, giving it a new name. My favorite breed 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. For no other reason than whim, let’s start at or near the beginning of this tract, where the esophagus meets the stomach. This is where a sphincter exists, that is supposed to keep 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.

Esophagus Affliction— Congenital esophageal achalasia is also known by many other names such as cardiospasm, megaesophagus, 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 convincing enough for her. While reportedly only about one percent of the dog population may be involved, mortality rate in pups is fairly high. Even when PRAA (Persistent Right Aortic Arch) has been ruled out as the cause, I believe the percentage 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.

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 or asphyxiate, due to progressive malnutrition, aspiration pneumonia, vomitus obstructing the air passage, and owner frustration over the regurgitation. Most adult cases that are presumed to be acquired have no cause discovered, which leads me to believe it is simply a milder form of the genetic problem that causes death by starvation in most pups between 5 and 8 weeks of age. Some veterinary references, however, stoutly consider these genetically/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.

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. The pedigree study in my GSD book gives food for thought.

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 afterwards, and the opacity of the cocktail clearly shows where it is. In the normal pup, it will be moving into and through the stomach, but in the dog with megaesophagus, most of it will be seen collected in that 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.

Megaesophagus signs appearing at old age are not typical, but dogs with “very mild cases” 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 form that may be 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.

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. 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.

Following 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 is, 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.]

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. 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.]
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Vomiting and gastritis — Vomiting comes easily to dogs. Grass eating and subsequent vomiting give rise to all sorts of explanations, the most popular being that the dog was sick and ate the grass to help him throw up. Actually, excess grass is more likely the reason for the reflex action. Dogs mostly eat grass because they like the taste of it, just as with the case of garbage, but it does appear that individuals learn that too much can cause vomiting, so the intentional eating of grass to induce vomiting may come after experience. Gastritis, an inflammation of the stomach lining, can be caused by the ingestion of too much grass, garbage, or indigestible materials. It can also be caused by viral or bacterial invasion, but much more common, especially in pups, is the presence of endoparasites: tapeworms, roundworms, hookworms, whipworms, and coccidia. Actually, tapeworms or roundworms can fill up the belly to the extent that they back up and cause vomiting from sheer bulk. The initial treatment for gastritis or vomiting may be the withholding of food and administration of Kaopectate every four hours.

Torsion — Commonly called bloat, sometimes described as gastric dilation/volvulus (GDV), this is a terrifying and frequently fatal disorder that German Shepherds and many other deep chested dogs experience. A twisting of the entrance and exit to the stomach traps the food and gas. As the stomach swells, the twist is more unlikely to be relieved without veterinary help. Great strides in surgical treatment have been made, but the key to reducing the high mortality is still time. Recognize the symptoms and get the dog to a veterinary surgeon, preferably an emergency or trauma-oriented hospital. Simple dilation (swelling due to gas) may not be serious as long as the dog is able to pass food into the duodenum, but it has been estimated that 80 percent of all dogs that experience simple dilation will someday also have torsion.

Symptoms of torsion include a swollen, turgid abdomen; the sluggish action of the dog; his white, frothy, unsuccessful attempts at vomiting; and perhaps his scratching in the dirt to make a cool hole in which to lie down. Also, the spleen will feel like a hard lump. The spleen is normally wrapped around some of the stomach and therefore splenic torsion usually accompanies gastric torsion, sometimes occurs without stomach torsion. When either happens, the return of the blood that flows through the spleen is shut off, causing shock, the “immediate” killer.

The first thing your vet is likely to do is attempt to push a tube down the throat into the stomach so the gas pressure can be relieved. If he cannot get past the twisted part of the alimentary canal, he may opt for immediate surgery so he can untwist the organs. One emergency veterinary service in the Detroit area uses a different kind of lavage tube in their treatment of acute torsion. The large diameter, stiff, black polyethylene pipe has a smaller, flexible tube inserted into it. This smaller tube is for warm water so that the stomach contents can be flushed out of the larger one for about fifteen minutes. In either case, once the dog has been stabilized, decisions can be made about whether to operate, or untwist a stomach or spleen still in volvulus.

Follow up surgical techniques are numerous, but perhaps the one with the most success in preventing future torsion is a tube gastrostomy. In this procedure, a rubber or vinyl tube is put into the stomach through the abdominal wall, and in a week the stomach wall at that point becomes attached with scar tissue to the peritoneum and abdominal wall. The tube is then pulled out. The surgical opening seals off in a few days, and since the stomach is fused to the abdominal wall, it is prevented from again twisting out of position. Regular gastroplexy, which is suturing the stomach to the abdominal cavity, is also widely performed. Because of these and other techniques, especially the rise of emergency clinics, the mortality rates among those that make it to the clinic while still alive has plummeted to about 15 percent. Another 15 percent or so die without being seen by the vet first.

Groups of scientists at many locations have been studying bloat for a long time, partly with help from such as Morris Animal Foundation, the GSDCA, and many others. So far, they have identified a number of likely causative factors, including behavioral traits. Breed susceptibility is pretty obvious, with 25 percent or more of Great Danes, Saint Bernards, Weimaraners, and Irish Setters expected to suffer from bloat sometime during their lives. German Shepherd Dogs, Standard Poodles, Collies, and Gordon Setters are fairly high on the incidence lists, also. Some of the characteristics seen most often in dogs that had bloated include some stressful event, even minor, in approximately the eight hours prior to the incident, a fearful temperament, and consumption of fairly large quantities of non-food material. The only dogs I’ve had direct contact with that bloated were of impeccable character, but those may have been in the minority. Purdue researchers found no pattern in presoaking dry food or not, but a slight correlation between several smaller meals and less bloat. Others found no relation to soybean meal in the food, an early target of breeders looking for a primary cause. Adding vegetables and canned or meat scraps appears to help lower incidence. Most dogs (60%) bloated not immediately after vigorous exercise soon after a meal, but in mid- to late evening when resting or sleeping.

Less likely are other types of torsion, but they can be as life-threatening. Splenic torsion can occur without gastric twisting, and an even more rare disorder is mesenteric root torsion. The mesentery is the white, fibrous, web-like or film-like tissue that connects the various sections of intestines to each other and to the abdominal wall. Blood vessels travel through the mesentery, and if there is a twisting there, regardless of whether the intestine itself is closed off, the blood supply can be halted and the intestinal tissue can become necrotic. Bloody diarrhea, vomiting, abdominal swelling and/or pain, and shock or general collapse can be symptomatic. It may be the same as what some call “twisted intestines”. So few dogs survive that it is impossible to prevent recurrence or conclusively predict whether those are at greater risk for another attack than any other dog is.

There is a familial element in torsion/volvulus in many, similar to the way cancer “runs in families”, but most cases don’t give a clue to hereditary factors. As in “toxic gut syndrome” which is also seen a lot in some GSD lines, it is almost impossible to tell which came first, the presence of abnormal bacterial populations and irritated intestinal or stomach linings, or the bloat itself. Which is cause and which is effect is not going to be easy or even possible to determine. Some investigators suspect that breeders may be stuffing their small, young puppies’ stomachs too much, with results that show up only later in life. Work goes on. Dr. Larry Glickman and his group at Purdue University as well as others have published several papers on this syndrome. Dr. Glickman commented that the supposed claim that raised bowls are correlated with increased incidence in torsion/bloat may just mean that this allows a dog to swallow more food (and air?) more quickly than if they were on the floor. A couple of website references, such as <http://www.vet.purdue.edu/epi/bloat.htm>, had some info, including from JAVMA’s Nov 15, 2000 issue. An abstract follows:

Canine Gastric Dilatation-Volvulus (Bloat)
School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907-1243
Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs. Lawrence Glickman, VMD, DrPH; N.W. Glickman, MS, MPH; D.B. Schellenberg, MS; M. Raghavan, DVM, MS; T. Lee, BA
Summary of findings (references 1 & 2) -A 5-year prospective study was conducted to determine the incidence and non-dietary risk factors for gastric dilatation-volvulus (GDV) in 11 large- and giant-breed dogs and to assess current recommendations to prevent GDV. During the study, 21 (2.4%) and 20 (2.7%) of the large and giant breed dogs, respectively, had at least 1 episode of GDV per year of observation and 29.6% of these dogs died. Increasing age, increasing thorax depth/width ratio, having a first degree relative with a history of GDV, a faster speed of eating, and using a raised feed bowl, were associated with an increased incidence of GDV. Table 1 summarizes the magnitude and direction of GDV risk associated with having each of these factors. The relative risk (RR) indicates the likelihood of developing the disease in the exposed group (risk factor present) relative to those who are not exposed (risk factor absent). For example, a dog with a first degree relative with a history of GDV is 1.63 times (63%) more likely to develop GDV than a dog without a history of GDV. As another example, if dog ‘A’ is a year older than dog ‘B’, then dog ‘A’ is 1.20 times (20%) more likely to develop GDV than dog ‘B’.

Most of the popular methods currently recommended to prevent GDV did not appear to be effective, and one of these, raising the feed bowl, may actually be detrimental in the breeds studied. In order to decrease the incidence of GDV, we suggest that dogs having a first degree relative with a history of GDV should not be bred. Prophylactic gastroplexy appears indicated for breeds at the highest risk of GDV, such as the Great Dane.
OBJECTIVE: To identify non-dietary risk factors for gastric dilatation-volvulus (GDV) in large breed and giant breed dogs. DESIGN: Prospective cohort study. ANIMALS: 1,637 dogs 6 months or older, of the following breeds: Akita, Bloodhound, Collie, Great Dane, Irish Setter, Irish Wolfhound, Newfoundland, Rottweiler, Saint Bernard, Standard Poodle, and Weimaraner.
PROCEDURE: Owners of dogs that did not have a history of GDV were recruited at dog shows, and the dog’s length and height and the depth and width of its thorax and abdomen were measured. Information concerning the dog’s medical history, genetic background, personality, and diet was obtained from the owners, and owners were contacted by mail and telephone at approximately 1-year intervals to determine whether dogs had developed GDV or died. Incidence of GDV, calculated on the basis of dog-years at risk for dogs that were or were not exposed to potential risk factors, was used to calculate the relative risk of GDV.
RESULTS AND CLINICAL RELEVANCE: Cumulative incidence of GDV during the study was 6% for large breed and giant breed dogs. Factors significantly associated with an increased risk of GDV were increasing age, having a first-degree relative with a history of GDV, having a faster speed of eating, and having a raised feeding bowl. Approximately 20 and 52% of cases of GDV among the large breed and giant breed dogs, respectively, were attributed to having a raised feed bowl.

Another article based on the same research but with slightly different data pulled out for the particular subject matter, was published in 1997: Multiple risk factors for the gastric dilatation-volvulus syndrome in dogs: a practitioner/owner case-control study (by): Glickman LT, Glickman NW, Schellenberg DB, Simpson K, Lantz GC. JAAHA, May-Jun., 1997. ABSTRACT: A study was conducted of 101 dogs (i.e., case dogs) that had acute episodes of gastric dilatation-volvulus (GDV) and 101 dogs (i.e., control dogs) with non-GDV-related problems. The control dogs were matched individually to case dogs by breed or size, and age. Predisposing factors that significantly (p less than 0.10) increased a dog’s risk of GDV were male gender, being underweight, eating one meal daily, eating rapidly, and a fearful temperament. Predisposing factors that decreased the risk of GDV significantly were a “happy” temperament and inclusion of table foods in a usual diet consisting primarily of dry dog food. The only factor that appeared to precipitate an acute episode of GDV [in their observations] was stress.

This contradicted the early-1990s study that indicated the opposite: that raised bowls should reduce the incidence of torsion/bloat. An article in “Bloat News” indicated a possible link that raised feeders might help prevent future episodes in a dog susceptible to “aerophagic” bloat (linked to swallowing too much air with the food, a commonly blamed cause at the time. Another issue of the same periodical indicated the single highest correlating factor was morphology (body type). A graph showed a sharp incidence increase as the depth of the chest exceeded its width and a strong correlation with body condition and temperament (weak nerves vs. calm, unstressed dogs). It may be good to select dogs that have strong, calm nerves, and are not slab-sided!

An article on the Foster and Smith Pet Education site, “Interpret Findings of a New Study on Bloat (Gastric Dilatation/Volvulus - GDV) with Caution”, December 2000, at: <http://www.peteducation.com:80/article.cfm?cls>, starting with a subheading, “The Question of Raised Food Bowls” circulated among fanciers. An excerpt: “In this study, when analyzing the association between the rate of GDV and the height of the food bowl some questions arise. First, the study found that large breed dogs whose food bowls are not elevated have the lowest risk of GDV. A confusing finding is that large breed dogs who have their bowl raised over 1 foot have the next lowest risk, and those who have their food bowl raised somewhere between the floor and one foot have the highest risk. So, the risk of GDV is not proportional to the height of the food bowl. If height of the food bowl is important, why doesn’t the risk steadily increase, the higher the food bowl is raised? Secondly, it appears that the researchers did not consider the height of the animal in relationship to the height of the bowl when looking for an association between food bowl height and prevalence of GDV. It would be of interest to compare the height of the bowl to the height of the dog, since dogs in this study varied widely in height due to breed differences and age (some were only 6 months old).

The third question is, ‘why weren’t similar findings obtained in giant breed dogs?’ In giant breeds, dogs with food bowls raised less than one foot had the same incidence of GDV as those dogs who did not have their dishes raised at all. Finally, it is unclear if the researchers also analyzed whether the elevated feeders were being used because other medical problems were present or if the elevated feeders could influence other factors such as the speed of eating. Could these medical problems or other factors, rather than the elevated feeders, have contributed to the increase in GDV in this group? A second subheading was ‘Comparison to Other Studies’: The results of this study agree with most previous studies, which also found that GDV increases with age. On the other hand, in several studies, dogs who ate faster had higher rates of GDV. In this study, we had a peculiar finding: eating at a fast rate was associated with an increased rate of GDV in large breed dogs, but a decreased rate in giant breed dogs. There have been other contradictory findings in research on GDV. In some studies it was found that overweight dogs had higher rates of GDV, and in other studies, lean dogs had higher rates. In this study, weight did not seem to make a difference. In most studies, including this one, the rate of GDV between males and females were similar; in one study, however, males had an appreciably higher rate.”

One other item that was brought to light on a “VetMed” e-mail discussion list, was that there is no proven advantage to raised feeders, and that the Foster and Smith company which runs the Pet Education website sells many types of elevated feeders.

While some excellent work on GDV has been carried out at Purdue, some feel that very little research has been done in the US on canine torsion/volvulus. Here are websites I was told will give information on GDV; I have not checked these out, so I cannot verify their usefulness. Some may be “foreign links, as well as human links and livestock links” as the person who gave me this list said:

http://www.editoraguara.com.br/cv/ano5/cv29/cv29.htm#tormes
http://www.vetinfo.com/dbloat.html#MesentericVolvulus
http://www.canismajor.com/dog/bloat.html
http://www.harkleen.com/Chimo.htm
http://search.atomz.com/search/?sp-q=mesenteric&sp-a=000608a5-sp00000000
http://www.emedicine.com/emerg/topic311.htm

The huge retrospective epidemiological study of GDV, as I mentioned above, is at Purdue, run by Larry Glickman. http://www.vet.purdue.edu/epi/bloat.htm The project was funded by the AKC Health Foundation and by breed clubs.
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Pancreatic Disorders —Very close to where the stomach empties its contents into the small intestine, ducts contribute secretions from the gall bladder and pancreas, mostly to aid in the metabolism of fats, which are fairly resistant to action by gastric acid. If either gland does not function properly, this can result in loose stools, and inefficient absorption of nutrients with highly variable severity.

The pancreas is a rather long, V-shaped gland located near the stomach, and aids the digestion of food. It has two major types of cells or tissues. One group is endocrine in nature, which means it secretes hormones into the circulatory system, which in turn transports them to other glands and body parts. The endocrine activity of this gland serves to control blood sugar level, and when defective, results in diabetes. The other part empties a group of biochemicals into the digestive tract. It produces enzymes and bicarbonate, and excretes these into the duodenum. One major enzyme, amylase, breaks down the long starch macromolecules, while others break down fats and proteins. Most GSD people, in America, at least, are concerned more with the digestive function than with diabetes. I have corresponded with fanciers in England who are concerned about pancreatic insufficiency, and since many of their lines are from recent German imports, this is possibly a more widespread problem there than I had earlier suspected.

Clinical pancreatitis — The word clinical may be used to mean “frank” or “obvious”, at least to a veterinarian with the training and equipment. Any disorder with “-itis” on the end refers to an inflammation. Most causes of this disorder are of unproven origin, but “bad genes” must be the prime suspect. Adult clinical pancreatitis is not tremendously common in the German Shepherd Dog, but when it does occur it is usually the middle aged, obese bitch on a fatty diet that has it. Chronic pancreatitis symptoms include emaciation, dull dry coat, and high appetite with poor digestion as seen by fatty, loose stools containing undigested starches. Treatment is aimed mainly at correcting the diet, but it is very difficult to control.

Pancreatic atrophy — On the other hand, German Shepherd Dogs seem to have a considerable predisposition to pancreatic atrophy, also known as juvenile atrophy or pancreatic insufficiency (PI), and certain bloodlines have been much more associated with it than others. For years I have referred to the milder manifestations as subclinical pancreatitis, because people who are not familiar with familial and breed tendencies are likely to miss the subtle signs, and I had suspected the two forms were variations of one basic problem. The disease usually starts before the dog is one year old, though many are three before symptoms are noticed. When lack of “drive”, diminished coat lustre, coprophagia, and/or poor weight are seen, have the stool examined by your veterinarian for abnormal fat level and absence or low level of the trypsin enzyme. If the problem is discovered before it becomes severe and chronic, Viokase™, a brand of powdered raw pancreas, added to the food half an hour or more before feeding usually produces good results. Other similar products that I am familiar with are called Pancreazyme™ and Prozyme™. I have heard of a British product called Tryplase as well. I was told, but have not verified this, that Prozyme “is not the medication of choice as it only contains the vegetable type enzymes.” Costs vary widely among these. Getting enough to do the job without making the owner go broke is a tough balancing act, though. By the way, these types of preparations also appear to be good for non specific diarrhea. I believe there is a strong possibility that subclinical pancreatitis can worsen with neglect into an acute attack by enzymes on the pancreatic and surrounding tissues themselves, and that this condition may be the cause of many instances of diagnosed perforated ulcers. Texas A&M vet school at one time was trying to get AKC and GSDCA funding to study and possibly identify a genetic marker for pancreatic acinar atrophy in the breed.

The Animal Health section of HelpLine (UK), autumn 1999 issue had several articles on frank pancreas insufficiency and malabsorption. That reported on a test for the specific detection of pancreatic insufficiency, using a trypsin method (TLI) from a single blood sample. This replaced the fecal test, which had proved inaccurate. Differential diagnosis of pancreatic insufficiency and other small intestine disease are sometimes difficult since clinical signs can be similar. Many problems that befall the GSD point to autoimmune conditions; research was carried out by Dr. D. Williams in the U.K. Pedigrees have been requested by veterinarians working on this problem, and a clearinghouse for information has been set up by Dorothy Cullum, 15 North Road, Brentwood, Essex, England. Chronic intestinal disease, called overgrowth of intestinal bacteria in the UK, and probably the same thing that the U.S.’ Dr. Chuck Kruger dubbed “toxic gut syndrome”, is also being studied in Britain, and has been found to be a particular problem in young dogs. Treatment with high dosage of antibiotics over a long term has been claimed to have a good success rate.

Malabsorption or poor digestion and 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. These symptoms can be caused or 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. I know that my strongest-character dogs over the years have also been able to eat almost anything without diarrhea. Others have also proffered the theory of an abnormality in the immune system. Such dogs are apparently more likely to show symptoms like increased susceptibility to bacteria, intolerance to change in diets, ravenous appetite, reduction in body weight or failure to gain, diarrhea, greasy-looking feces with possibly undigested cellulose as well, and an “unthrifty” dry coat. The usual response by breeders and vets is to try the enzyme supplements and/or something like Hills Prescription Diet. But there are about as many stories of failure as there are of successful (though tricky, difficult) control. Some believe that an increase in roughage or “bulk” is needed in order to “keep the food in the system” long enough for the digestive system to do its work, but others say that more bulk or roughage tends to move the contents along a little faster. Also, we are told to feed our affected dogs low-fat foods.

Some owners with access to slaughterhouses claim some benefit from feeding raw pancreas, but there is not enough data with scientific controls to consider this anything more than anecdotal testimony. This is not to discount testimonials, though, as these can lead to success and may be incentive for scientific corroboration. One reader in the UK tried the natural pig pancreas plus roughage route, and said, “It [pancreas from the abattoir] is no more unpleasant to handle than any other meat from the freezer, costs half the price of powdered enzymes, the dog absolutely loves it and appears to be more effective than any man made preparation on the market! He is not requiring as much food, as he is obviously absorbing what he needs from his diet now. He is not full of wind, and he is now producing approx. 1/3 of the amount of faeces that he did on the powders. I have also noticed that he is no longer ravenously hungry and has actually left some of his dinner on a few occasions.” On the other hand, many experts say that you should reduce the amount of non-digestible fiber in the diet for dogs with pancreas problems.

If you choose the expensive specialized EPI diet foods from Hills, Eukanuba, or others, check the labels and prices — they are “out of sight”. People who treat their EPI dogs for the rest of the dogs’ lives can spend about $1,000 to $1,500 annually for the enzymes alone. If you go along this road, you will have to “soak” the ration for a while, to give the enzymes time to work — longer for the dry rations than for the canned. The enzymes have their greatest effect after about 20 minutes.

Warning: you can spin your wheels for years on the abundance and infinite variety of nutritional advice. Many claims are entirely unrelated and coincidental to results, but people who are desperate will tend to try them all. One correspondent told me that, after initial help, she was no longer getting satisfaction by using just the enzymes; her dog’s stools were getting poor again. Later, she found good maintenance results by supplementing with folate, vitamin B-12, banana, live-culture yogurt, oatmeal, baked yams, and flaxseed oil twice a day, in addition to “one Cimitadine tablet (brand name is Tagamet) morning and evening three times a week”. (Cephaloxin 500mg two or three times daily, depending on the situation, is sometimes administered for two weeks.) This diet change had followed the Texas A&M College of Vet Medicine’s suggested treatment with cobalamine folate. Cobalamine is vitamin B-12, and folic acid (obtained synthetically or in liver, green leaves, and yeast) is essential to the friendly lactobacillus in the gut, in combination with which it inhibits malabsorption. That lady did not see a turn-around in condition until more B-12 was added to the vet school’s recommended treatment. She found that 2,000 milligrams of folate and a fourth-teaspoonful of liquid B-12 with the dog’s light meals three times a day gave marked improvement It appears that occasional (quarterly, for example) antibiotic treatment to kill unfriendly bacteria, followed by folate and yogurt to encourage the lactobacillus, is highly thought of by veterinary nutritional specialists. I am a fan of vitamin E, having seen benefits in many areas, so I always recommend that people also give one or two 400-IU capsules a day of Vitamin E to help boost the immune system.

Most people make a distinction between EPI (Exocrine Pancreatic Insufficiency) and pancreatitis, some saying that dogs can recover from pancreatitis, rather simple inflammation of the pancreas, and that when the pancreas begins to atrophy, the only thing you can do is supplement with digestive enzymes like Viokase V or with Pancreazyme. I tend to believe the two conditions are more intrinsically linked. Canned dog foods, even the non-prescription brands, are said to be easier for the EPI dogs to digest than is dry kibble. The EPI dog is unable to efficiently digest carbohydrates, protein and especially fat. The condition is also called acinar atrophy, the word “acinar” referring to the physical tissue structures that make up lobules in the gland. When the pancreas atrophies, it loses ability to function in its digestive mode; it apparently does not interfere with insulin production, which is its endocrine function carried on by different types of cells. Some dogs do become diabetic as well, but this may be entirely unrelated.

I have been told that the statistics on EPI dogs indicated that 1 in 5 pups born to an EPI-affected dam would eventually show signs of EPI. There seem to be a higher than average number of stillborn pups, as well. Whether this has anything directly (genetically) to do with EPI, or is a reflection on the poorer physical condition that leads to uterine inertia, is hard to say. By the way, on this website you are now surfing, you might also find my article on uterine inertia and the use of oxytocin.

The test that your vet or his contracted lab will perform will give you a reading of what is called Tli. This is an enzyme blood test that determines the level of digestive enzymes present. It can vary from day to day, increasing and decreasing and varying within the same day. The scale on this test from low to high, is 5.0 to 35.0 while GSD’s rarely test over the 5.0 to 8.0 range. At Texas A&M, the Researcher told me that they have found that dogs that normally test below 8.0 will most probably become EPI positive. Of course they are talking about all breeds, and we must remember that there are breed differences. The GSD, for example, has a higher packed-cell volume than other breeds, and it is likely the Tli range that is abnormal for others might be more normal for GSDs. The disorder might remain fairly unnoticed or asymptomatic until it reaches a Tli much below 5.0, then the dog typically begins to get voraciously hungry and has terrible diarrhea with a sour odor, many times a day. Severe weight loss is an indication that the dog is starving to death. The fur loses pigment and gloss, becomes dry and brittle and often is 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 is down around 2.5 to 3.0. In most breeds perhaps, any dog that tests at even an 8.0 will be at high risk for EPI. So, most dogs will be diagnosed with EPI when Tli is at 8.0 or less, and perhaps 0.4 or lower for GSDs. If a dog is found to be within the normal Tli range (for GSD’s 5.0 to 8.0) but exhibits symptoms such as much flatulence, diarrhea that is light brown/yellow to clay color from time to time, the dog should be tested for levels of Lipase, Protease and Amylase.

The genetics of pancreatic disorders may confuse, because the expressions are highly variable. Some can carry the trait and never develop EPI, while others show symptoms, although the genotype may be similar. The wisest recommendation is that such dogs not be bred as they most certainly carry the recessive gene. They are currently looking for a “marker” in the families of dogs they’ve been working with over the last couple of years. Before breeding, one perhaps should have the TLi test done, and get a hint of the possibility of carrying the gene. If you breed two that are carriers together, you risk as much as the entire litter having EPI. I once bought a full brother of a famous champion named Shiloh; My “Harry” was a beautiful animal with excellent hips, but he developed the pancreatic disorder and had to be controlled as much as possible with the enzyme powder. I had sold a co-ownership in him before the disorder developed, and he was killed in a car crash before years of treatment and follow-up would have been completed. Some others with close relatives also reported pancreatic insufficiency in their dogs. One vet I know of told his client that EPI “is not considered being ill — merely a genetic condition.” Merely a matter of semantics? To me, pancreatic insufficiency is an abnormality that calls for removal from the gene pool, whether the dog has a mild case or asymptomatic most of the time. I have found that most vets take but a modicum of hours of nutrition and practical genetics classes in vet school, and then forget most because they don’t use it every day. Breeders, especially those with a science background, are more reliable sources of information, I think. Unfortunately, not many people who offer their EPI males at stud 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?” Yes, in spite of the fact it is good for various causes of diarrhea, it is so much more expensive than Kaopectate, that it makes you wonder.

Connection between PI and GDV? — 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 who had “chatted” on the Internet with many GSD owners in the UK and the USA 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.”

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. The German Shepherd seems to experience a high incidence of this disorder and I believe there is a genetic propensity, a familial trait, in certain bloodlines.

Diarrhea and soft stool — Diarrhea can be a symptom of any number of disorders from cancer to overeating, but is most often associated with disease or parasitism of the small intestine. Diarrhea or loose stool is quite common in the German Shepherd Dog, even when no physiological disease has been identified. However, since this is not a normal condition, the owner should make a sincere attempt to find and attack the cause. Some of the causative factors in true diarrhea are: pancreatic insufficiency, chemical or mechanical irritation of intestinal linings, parasites, microorganisms, and a psychosomatic condition related to the “high-strung,” emotional make-up of the German Shepherd Dog. Foods that can cause loose stool include milk (if suddenly introduced into the diet), excessive liver, fats, and those with a high fiber content. However, simple overeating is perhaps the most frequent culprit. Most people overfeed their dogs.

Soft to runny stools may be an indication of a general inflammation of the stomach and intestines known as eosinophilic gastroenteritis. It is treated symptomatically with something to coat the lining, plus perhaps a steroid and Kaopectate, until the dog “heals itself.” Many veterinarians and owners administer Pepto-Bismol, also. In the case of very young puppies with watery stool or repeated diarrhea, rush to your veterinary clinic with the pup and the stool samples. Most of the time the cause of diarrhea in a young puppy is serious, such as parvo or coccidiosis, perhaps with hookworm as well. The Campylobacter bacteria cause some cases of acute or chronic diarrhea, and most labs would have no trouble identifying this infection. Generally watery diarrhea is not an indicator of “campy”. Erythromycin antibiotic is 90% effective, although resistant strains may be evolving.

Even giardia can be quite dangerous, if the pup is young and has been exposed to other challenges, such as being wormy, stressed, or otherwise weakened. Giardiasis is marked by watery diarrhea with a uniquely acrid “bloody” odor, that experienced breeders can identify quite easily even before a stool sample is analyzed. Giardia is a protozoan disease; i.e., it is caused by a single-celled “animal” flagellate parasite, so-called because it is highly motile, having a tail. The Merck Veterinary Manual describes it: “Transmission occurs in the cyst stage by the fecal-oral route. Incubation and pre-patent periods are generally 5 to 14 days. Giardia cysts survive in the environment and thus are a source of infection and reinfection for animals, particularly those in crowded conditions... prompt removal of feces from cages, runs, and yards will limit environmental contamination. Cysts contaminating the hair of dogs and cats may be a source of reinfection.” Regarding treatment, the manual says “Flagyl ™ (metronidazole) is about 65% effective” (in removing cysts from feces) and if administered “for 3 days, effectively removes giardia cysts from feces of dogs; no side effects are reported.” By the way, these oocysts are much smaller than worm eggs, and require much higher magnification to find them; still, they are not shed every day, so it may be wise to start treatment and then wait for a three-to-five-day combined stool sample to be checked by your vet. Despite the “low” rate or ridding the body of cysts, many vets prefer Flagyl. The success rate is reportedly declining as giardia is now demonstrating resistance to the drug. In addition, it may be a little hard on young puppies, with some neurological side effects.

Panacur (fenbendazole) is relatively pricey and seems to be sold only in large-volume jars from the usual vet supply catalogs. For giardia, Panacur is considered a static drug, 100% effective in clearing cysts from feces in 3 days (the cysts are the infective part), with no side effects reported, and is safe for pregnant and lactating animals. In the lab, giardia did not develop resistance to fenbendazole. It does not have a repelling taste. A field representative for Intervet, the company that manufactures Panacur, admitted that Flagyl may be preferable for the occasional dog that has general stomach distress. With either one, a 5-day dose has been reported by some to be effective when the 3-day regime was not.

I would also recommend that you ask your vet about Albon™ (sulfamethoxine) which is much more effective, although for a different reason, and should be given for 15 to 21 days. The sulfa drugs do nothing to the Giardia organism itself, but they do combat the secondary bacterial infections that are probably the real killers of puppies. Such an approach allows the pup to regain enough health to withstand the protozoan, even though it may be retained in the body for a while. It is more readily available, probably lower in cost, and in widespread use. A disadvantage in any sulfa drug is a number of adverse side-effects, but I have not had any problems, probably because I do not keep dogs on the medication longer than recommended, and have genetically strong breeding stock.

There are a few less-often used: Valbazen (albendazole) is about 90% effective in removing cysts but has been implicated in birth defects, suppression of the immune system, and destruction of red blood cells. .Atabrine (quinacrine) also has unpleasant side effects. Some have recommended a Giardia Lamblia vaccine for dogs with persistent or repeated cases.

Toxic gut syndrome (TGS) — This disorder has been identified as a specific syndrome, with some similarities to other disorders such as intestinal volvulus, which may have been blamed for death when TGS was the real villain. The German Shepherd Dog has a higher packed cell volume (number of blood cells per unit of blood) than do most other breeds, with 50 to 60 percent “solids” compared with 40 to 45 percent. When such a dog becomes dehydrated, thickened and/or lessened blood supply to the small intestine increases growth of bacteria that are always present there. These Clostridium and E. cold bacteria produce such quantities of toxins that the dog is unable to get rid of them fast enough, and death by poisoning occurs. By the time owners see symptoms such as discomfort when the abdomen is touched, attempts to vomit, and excessive salivation, it is probably too late. Prevention may be accomplished through dietary means (feeding Lactobacillus acidophilus, yogurt, or cultured buttermilk), or by the same toxoid vaccine that is given to lambs to prevent Clostridium perfringens types C and D. As research is done on this recently defined syndrome, more will become known as to the best treatment.

Other problems — Ulcers have been diagnosed too frequently in German Shepherds and may be related to pancreatic problems or other causes: it’s difficult to tell, when several conditions exist at once, whether one is the cause or effect of another. Necrotic bowel syndrome, a disorder of unknown cause, is diagnosed usually on autopsy, when part of the intestine is found to be dead and rotting away. This condition may be synonymous with or overlap intussusception or other diseases. It takes a small toll, mostly among heavily linebred German Shepherd Dogs.

Eosinophilic ulcerative colitis — This syndrome is most common in Cocker Spaniels and German Shepherd Dogs. If your pup or adult has intermittent to constant diarrhea, with or without blood, and does not respond to treatments for the more common disorders, this disease may be the cause. Initial treatment may include corticosteroids, antibiotics, and antispasmodics to see if the symptoms can be halted.

Irritable colon — Also known as spastic colon, this disorder with mucus in or on the surface of soft or frequent stools may be the result of stress. The best cure is prevention — breed stable temperaments and build confidence in puppies.

Polyps — Rectal polyps are little round or teardrop shaped red to purplish balls. Sometimes they are clustered like tiny grapes, and are found very close to the anal opening or further inside the rectum. They should be surgically removed, since they rupture easily and are a potential site for infection. A drop of bright red blood recurring on the end of stools is a sign that you should have the dog examined for polyps.

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The author is a breeder since 1945, a teacher and lecturer in canine topics, and dog show judge. His book, The Total German Shepherd Dog, is available from http://www.Hoflin.com and he can be contacted at Mr.GSD@Juno.com