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Canine Gastrointestinal
Disorders
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Gastrointestinal Disorders in the GSD and Several Other
Breeds
Canine Digestive Tract Disorders - part 1 - Fred Lanting
Canine Digestive Tract Disorders - part 2 - Fred
Lanting
Canine Digestive Tract Disorders - part 3 - Fred Lanting
Gastrointestinal
Disorders in the GSD and Several Other Breeds
Fred Lanting ©1990
Oesophagus — Congenital oesophageal achalasia is also known
by many other names such as cardiospasm, mega?esophagus, dilated oesophagus,
and ectasia. The disorder appears to be caused by a simple autosomal recessive
in German Shepherds, although it is highly variable in expression. While
reportedly only about one percent of the dog population may be involved,
mortality rate in pups is fairly high. Even when PRAA has been ruled out
as the cause, I believe the percentage in German Shepherds is quite a bit
higher than the 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.
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 oesophagus
problems, peripheral neuropathies, gastric dilation with or without torsion
and especially myasthenia gravis. Even in adults, many are euthanised
or asphyxiate due to progressive malnutrition, aspiration pneumonia, 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. A loss of peristaltic action
(that contraction that squeezes the food downward like a cow being milked)
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.
Symptoms 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 oesophagus
on the way down, an affected pup's muscles apparently fail to contract
enough to prevent the food bolus from simply staying in a pouch just in
front of the entrance to the stomach. In time, the muscles become weaker
and even less able to squeeze the food ball, and even liquid food remains
in a hanging “pelican pouch” forward of the stomach entrance and below
it. As with PRAA, the pup becomes emaciated and listless, often dying of
starvation. In fact, the two conditions may be indistinguishable without
autopsy. The accompanying pedigree study gives food for thought.
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 oesophageal dilation, affecting various breeds
to different extents. However, German Shepherds have over thirteen times
the incidence of oesophageal disorders of all other breeds combined, though
PRAA may be part of this statistic.
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 eat grass because they like the taste of it, just as with the
case of garbage. 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
withholding food and administering Kaopectate every four hours.
Torsion — Commonly called bloat, sometimes described as gastric
dilation/volvulus, 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, and 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 accompanies
gastric torsion. When this 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 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 rate 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 behavioural 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 pre
soaking 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.
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. 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
diarrhoea, 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.
Intussusception— In young pups (and other animals including humans)
the intestine can invaginate (one part slips inside another). The condition,
also referred to as "telescoping intestines," occurs in adults, too, 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.
Diarrhoea and soft stool — Diarrhoea 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. Diarrhoea 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 diarrhoea are: pancreatic insufficiency,
chemical or mechanical irritation of intestinal linings, parasites, micro-organisms,
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), liver, fats, and those with
a high fibre content. However, simple overeating is perhaps the most frequent
culprit in adults.
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
administer Pepto-Bismol, also. In the case of young puppies with watery
stool or repeated diarrhoea, rush to your veterinary clinic with the pup
and the stool samples. Most of the time the cause of diarrhoea 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 diarrhoea,
and most labs would have no trouble identifying this infection. Generally
watery diarrhoea is not an indicator of “campy”. Erythromycin antibiotic
is 90% effective, although resistant strains may be evolving.
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 number of blood
cells per unit of blood than do most other breeds, with 50 to 60 percent
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, yoghurt, 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 line bred
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 diarrhoea, with or without blood, 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.
Anal glands — Occasionally, anal sacs may become infected, and
the dog may scoot along on the ground, rubbing his rump in an effort to
relieve the itch. This won't help, but you can easily "express" these glands.
Lift the tail high with almost enough effort to lift the dog's rear off the
table or floor, and very firmly pinch the sphincter including the sacs. Be
sure to use a couple of layers of paper towel or some cotton to keep the
liquid from squirting across the room or on you. Most dogs do not need attention
nearly as much as owners think they do.
Perianal fistulas — Known by a number of names, these abnormal
passages between two surfaces or an opening to the exterior, in the area
of the anus, is a condition seen more in German Shepherds than in other
breeds. While probably familial or congenital, the disorder is thought by
some to be caused by an injury or an abscess. More likely, however, it reflects
an immune system weakness. Symptoms include frequent licking or biting at
the "vent," and a bad odour and pus may also be seen. If untreated, ulceration
will develop. Only fair results have been reported with cryotherapy, which
is freezing with liquid nitrogen or nitrous oxide. Since some veterinarians
prefer to use familiar surgical procedures rather than cryosurgery, ask for
a second opinion if you aren't sure, especially at a veterinary college clinic.
Frankly, the prognosis has historically been very poor; there has not been
a high satisfaction rate regardless of treatment method. But a pharmacological
approach has come to the foreground in the late 1990s, that being the use
of the immuno-suppressive drug cyclosporine in an oil base, fed twice a
day for as long as 5 months. It has had some success so far, though researchers
warn that remission of symptoms may not be permanent in all dogs (nor is
it in the case of surgery), and this immunosuppressive treatment is extremely
expensive, thanks not only to the drug but also to close monitoring by
the veterinarian. However, even in those dogs not “cured” by the drug alone,
it improves the condition of the lesions enough so that surgery is much
less extensive and has a better chance of success.
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.
The Pancreas
The pancreas is a rather long, V?shaped gland that 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 other
group empties into the digestive tract. Located near the stomach, it produces
enzymes, bicarbonate, and hormones; the first two are delivered to the intestine,
the third is secreted into the bloodstream. One major enzyme, amylase, breaks
down the long starch macromolecules, while others break down fats and proteins.
The endocrine (glandular) portion of the pancreas, which does not excrete
into the alimentary canal but rather secretes into the circulatory system,
functions in control of blood sugar level, and when defective, results in
diabetes. Most GSD people, in America, at least, are concerned more with
the digestive function than with diabetes. Just before publication, I also
heard from 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 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. Most causes of this disorder are of unknown origin. 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 accomplished mainly by
correcting the diet.
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, and certain bloodlines
have been much more associated with it than others. For years I have referred
to it as subclinical pancreatitis, because people who are not familiar
with familial and breed tendencies are likely to miss the subtle signs.
The disease usually starts before the dog is one year old, though many
are three before symptoms are noticed. When lack of "drive," less 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. Another
similar product is called Pancreazyme™. 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 are also good for non specific diarrhoea. 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. 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 is trying to get AKC and GSDCA funding
to study and possibly identify a genetic marker for pancreatic acinar atrophy
in the breed.
back to top
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Canine Digestive Tract Disorders
Polyps
Megaesophagus Torsion Bloat (Volvulus)
Pancreatic Insufficiency PART 1
Fred Lanting
Canine Digestive Tract Disorders
in Several Breeds
INTRODUCTION
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 favourite 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:
Megaesophagus
Torsion/Bloat (Volvulus)
Pancreatic Insufficiency (EPI)
Oesophagus Affliction
For no other reason than whim, lets start at or near the beginning
of this alimentary tract, where the oesophagus 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, side
tracked 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 oesophageal dilation, affecting various breeds to different
extents. However, German Shepherds have over thirteen times the incidence
of oesophageal 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 oesophageal 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 oesophageal constriction, hypothyroidism, hypoadrenocortcism,
oesophagi's, thymoma (tumour of the thymus gland), thallium (a metallic
element), and lead toxins.
Congenital megaesophagus occurs in young dogs and is a developmental
abnormality of the oesophagus. Megaesophagus-susceptible breeds include
Irish Setters, German Shepherd Dogs, Golden Retrievers, Shar Peis, Great
Danes, Miniature Schnauzers, Wire haired 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, oesophageal achalasia, dilated oesophagus, 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 euthanised 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 oesophagus problems, peripheral neuropathies,
gastric dilation with or without torsion, and especially myasthenia gravis.
Even in adults, many are euthanised 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 oesophagus,
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 oesophagus
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 sulphate 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 oesophageal
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 oesophagus 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
oesophageal 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 euthanised.
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 oesophagus. 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 litter mates or offspring (a fact you
may never know). The math is simple. Lets say you breed a bitch with affected
litter mates. Her risk to be a carrier is 2/3. You decide to breed her back
to her paternal grand sire. 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 = granddads risk to
be a carrier). This assumes that the grand sire has no affected litter
mates or offspring. So the chance for each pup produced by this mating
to be affected is: bitch’s risk to be a carrier x dogs 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 litter mates 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 out crossed 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 litter mate is really affected
but asymptomatic, and could still have affected pups. Therefore, the risk
that one of the unaffected litter mates 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 litter mates as amount of grey
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) litter mates 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 oesophagus, 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 oesophageal 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 litter mates 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 haemophilia or epilepsy was
in England just a couple decades ago, and since it has not noticeably diminished
in line bred 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 cant 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
behavioural 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 litter mates 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.]
back to top
***********************************
Canine Digestive Tract Disorders
Polyps
Megaesophagus Torsion Bloat (Volvulus)
Pancreatic Insufficiency Part 2
Fred Lanting
Continued from PART
1
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 behavioural 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 pre soaking 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 diarrhoea, 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 much of 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 food 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. The table below 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’.
Risk Factor Relative
Risk Interpretation
Age 1.20% increase in risk for each year increase in age
Chest depth/width ratio
(1.0 to 2.4)2.7% increase in risk for each unit increase in chest depth/width
ratio
First degree relative with
GDV (yes vs. no) 1.6363% increase in risk associated with having a
first degree relative with GDV
Using a raised feed bowl
(yes vs. no) 2.10110% increase in risk associated with using a raised
food bowl, contrary to popular opinion!*
Speed of eating (1-10 scale)
[for Large dogs only] 1.1515% increase in risk for each unit increase
in speed of eating score for large dogs
*studies may be ongoing to clear up this concept.
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. [Gastroplexy
is a procedure that by surgery and scar tissue formation affixes various
surfaces to each other to reduce chance of twisting.]
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 dogs length and height and the depth
and width of its thorax and abdomen were measured. Information concerning
the dogs 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. [end of abstract]
************************************************
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 dogs 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 analysing 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 more than 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 analysed 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 insufficient 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://www.f-v-s.com/newsletters/vol1no2emergency.htm
http://web.missouri.edu/~vmicrorc/Nematoda/Strongylids/Strongyles/Svulgaris.htm
http://search.atomz.com/search/?sp-q=mesenteric&sp-a=000608a5-sp00000000
http://www.aevedi.org/00121CV.htm
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, exocrine,
part empties a group of biochemicals into the digestive tract. It produces
enzymes and bicarbonate, and excretes these into the duodenum, which is the
first short section of the small intestine. 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. I know I have seen the occurrence
in pancreatic insufficiency increase among the German lines in the U.S.,
but that might be because more and more people are turning away from the
American GSD for many other reasons.
Exocrine pancreatic insufficiency (EPI) is a condition in which
that part of the pancreas stops producing and secreting enough digestive
enzymes and bicarbonate to properly digest food in the small intestine.
Severity may vary between individuals, and even vary in one dog from time
to time. Diarrhoea and foul smelling faeces due to high undigested fat mark
the condition known as steatorrhea, and because food ingredients are not
being digested the animal becomes malnourished; in many cases nutritional
deficiency as well as energy deficiency results. The cause of EPI can sometimes
be traced to another primary pancreatic disease, or from any disease that
interferes with enzyme secretion or action in the intestine. Juvenile pancreatic
atrophy and chronic pancreatitis are the most common, but other causes include
obstruction of the pancreatic duct (by a tumour, for example) which ordinarily
carries the enzymes into the lumen of the duodenum.
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. Symptoms of chronic pancreatitis
(recurrent inflammation of the pancreas) 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 sub clinical 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. EPI can be sub clinical for many months or even years
before it worsens or is classified as chronic and acute. 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 diarrhoea. I believe there is a strong possibility
that sub clinical 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 cause of pancreatic acinar atrophy has been determined
to be an immune system deficiency.
Malabsorption or poor digestion and stool condition are frequently
seen in the GSD, and in my experience, has been more so in the heavily
line bred 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 sub clinical 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 diarrhoea. 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, diarrhoea, greasy looking faeces 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 make it
harder to control. Also, we are told to feed our affected dogs low fat foods
but not deprive them of the essential fatty acids.
The Animal Health section of HelpLine (UK), autumn 1999 issue had several
articles on frank pancreas insufficiency and malabsorption. It reported
that the trypsin method (Tli) replaced the faecal 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. in this regard.
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. For further reading on the subject,
contact her:
mailto:dorothy-cullum@cermar.co.uk
Treatment
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 that the 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 fibre in the diet for dogs with
pancreas problems.
Treatment is nutritional — it involves the use of replacement pancreatic
enzymes given orally. 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 a soak of about 20 minutes.
Suitable products are available in powder or crushed non enteric coated
tablets. Enteric coated tablets are not usually recommended because dissolution
of the coating by alkaline pH in the intestine is unreliable. Because some
enzyme is denatured by acid in the stomach, premixing the enzyme supplement
with the food and left for about three quarters of an hour at room temperature
is sometimes recommended.
According to at least one commercial enzyme powder producer, ProVet,
medications such as receptor inhibitors (e.g. Cimetidine) can also be
useful because they reduce gastric acid secretion; thus, less pancreatic
enzyme is denatured during passage through the stomach. If bacterial overgrowth
is present, oral antibiotics may be indicated as well. With enzyme replacement
and cimetidine and/or neomycin, faecal fat concentrations can be returned
to normal.
The following dietary management is recommended by ProVet (mailto:info@provet.co.uk):
Feed a highly digestible, palatable, complete ration. Avoid home made
rations.
The ideal profile is a diet that is low in fat content, but contains
medium chain fatty acids; avoid foods with excess carbohydrate and low
fibre.
Feed multiple small meals (at least 3 times daily)
A dog owner wrote to me and said, “I want to try your recommendation
of fresh pancreas fed to the puppy with chronic diarrhoea. How much do
I give and how often? At every meal? And, I assume it is given raw.”
Given the variety of symptoms and needs of different dogs, it's impossible
to accurately measure how much enzyme the dog will need, or how much benefit
it may do him. Best bet is to treat raw or cooked pancreas as any meat
supplement: no more than 25% of the daily ration. Probably 10% is a good
starting point for experimentation. Just estimate. If you get better results
with larger percentage, go for it. Remember that there are many factors,
and the dog's needs may change daily. Keep other fats in the diet very
low... get a low fat but highly digestible commercial dry food as your
base. I would try 10% replacement with pancreas and another 10% with lean
meat like chicken. One problem with living in Alabama is regulations against
selling stuff such as over date cottage cheese, cracked eggs, organ meats,
etc. Residents of our fair state have to have a friend “on the inside” at
some slaughterhouse or wholesale butcher or manager of a store meat dep't.
Yes, raw is probably better, as cooking can destroy some enzymes. I think
the Viokase people freeze-dry their product so they can sell it as a ground
powder. Yes, I would feed it at every meal, so I would have it chopped,
cubed, or ground, and make patties to freeze, thawing out a couple every
day.
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. Another correspondent told me that, after initial help, she
was no longer getting satisfaction by using just the enzymes; her dogs
stools were getting poor again. Later, she found good maintenance results
by supplementing with folate, vitamin B-12, banana, live culture yoghurt,
oatmeal, baked yams, and flaxseed oil (for those fatty acids) twice a day,
in addition to “one cimetidine tablet (brand name is Tagamet) morning and
evening three times a week”. Cephaloxin 500 mg 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 dogs 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 yoghurt 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,
the 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 the website you are now surfing or may soon,
you might also find my article on uterine inertia and the use of oxytocin.
Diagnosis
Increased gut sounds are often noticed by the owner or the vet. Sometimes
we see a pallor in the gums due to anaemia and low concentrations of circulating
blood protein. But EPI diagnosis needs to be confirmed with lab tests.
The most used test for dogs is the Trypsin like immunoreactivity (Tli or
TLI) test, but other tests are often employed, and may still be needed
in complicated cases that have more than one concurrent disease. Microscopic
views of stool samples and lab tests for faecal fat are often used. The
Tli test that your vet or his contracted lab will perform determines the
levels of digestive enzymes like trypsin that are present. It can vary
from day to day, even 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
tells us they have found that dogs that normally test below 8.0 will most
probably become EPI positive.
Description
The TLI test is highly sensitive and specific for the diagnosis of
canine exocrine pancreatic insufficiency (EPI). This test measures the
concentration of trypsin like proteins in a blood sample by radio immunoassay.
These proteins diffuse into the blood stream in small amounts (0.01 0.
1% of pancreatic trypsinogen).
In normal dogs the TLI concentrations are greater than 2.5pg/L (up
to 35gug/L).
In dogs with exocrine pancreatic insufficiency TLI concentrations are
less than 2.5 pg/L
In dogs with pancreatitis TLI can be normal or increased.
Dogs with bacterial overgrowth have a normal TLI test unless exocrine
pancreatic insufficiency is present as well.
False negative results may occur if a dog has concurrent pancreatitis
(increasing TLI) and exocrine insufficiency
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 or manageable 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
diarrhoea with a sour odour, 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,
diarrhoea that is light brown/yellow to clay colour from time to time, the
dog should be tested for levels of Lipase, Protease and Amylase.
I had corresponded with a lady in Michigan named Dee, who had much
personal experience with EPI. She and others discovered that even if the
test shows the dog to be in the 8 range on the scale, it's quite likely
that the dog has developed EPI, or will in the future. Other breeds seem
to test higher, such as 15 to 35. GSDs are noted for having notoriously
low TLi's. The condition is widespread in the breed, probably due to considerably
tight inbreeding on “carriers”. The higher the reading is in a GSD, the
better; it indicates that the dog is digesting normally. Not all GSDs are
symptomatic, but any unexplained diarrhoea and weight loss, a voracious
appetite, frequent stools that are runny or like pudding in firmness, or
are pale coloured, such as putty grey, or dark mustard yellow, and of a
sour foul smelling type, are good reasons to have the dog Tli-tested, to
determine if the pancreas is failing. With this condition the dog is not
necessarily diabetic, as the condition does not affect the endocrine portion
of the pancreas. However, if the dog has also developed diabetes, then it
is extremely difficult to treat the dog, and one would wisely consider putting
his dog out of such a miserable state.
Dee says: “If one breeds one dog that is a carrier of the EPI gene(s)
to another who is also a carrier, it is most likely all the pups will be
affected. Statistics of a few years ago indicated that one in every five
pups will be affected if only one parent is “diagnostic” for EPI. Another
article said that one in four would be affected. This condition can show
up any time from birth on, if the pups come from parents who both carry
the gene for EPI. If only one parent is a carrier, then the odds of escaping
symptoms are improved. For this reason some recommend that only males be
given the TLi to see what range they are in, prior to breeding. If both dam
and sire are “testing low”, we would advise not breeding them. Only the
GSDs with the highest readings and without any "marker gene" should be bred.
Dee feels that the breeding pair should be tested at least twice before
being bred instead of finding the problem later, after one realizes that
they've produced litters of defective dogs that will die a terrible death
if not treated.
We must also consider the owner on limited income who cannot afford
to treat a dog for its lifetime, a dog that perhaps should be destroyed.
Even if the person can afford to treat the dog for its lifetime, but the
enzymes stop working, or are just plain ineffective, the dog will probably
still have to be destroyed. The TLi varies from time to time, so one will
not necessarily get the same reading twice, but if the dogs regularly test
low, castration or spay would certainly halt the genetic progression.
Being recessive, EPI is the kind of condition that one cannot easily “breed
out”. It's up to the good breeders to control this condition.
In general, many dogs who test at 8.0 have been known to develop EPI
as they get older. Apparently they are carriers, and may not necessarily
show symptoms early in life. Occasional bouts with diarrhoea may be insufficiently
diagnosed as idiopathic "gastroenteritis" at the time, and get treatment
that only temporarily seems to resolve the problem. Dogs with a history of
bloating/torsion and/or bouts of unexplained diarrhoea are reportedly quite
likely to be EPI-carrier suspects, although this observation is purely anecdotal.
EPI occurs most frequently in dogs, and rarely in cats. The German Shepherd
Dog is the breed most likely to be presented with EPI and/or pancreatic atrophy.
The popularity and high population of the GSD breed may be a factor in this
seeming phenomenon, and close inbreeding practices may have some influence.
It certainly seems that the American lines are plagued far more than the
German lines are. Some people perceive a probable connection or coincidence
between anal furunculosis (perianal fistulas) and EPI. A great deal of the
digestive system may be affected one way or another. In Finland, the Rough
coated Collie is also predisposed to develop EPI.
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 Paladen; 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 Viokase enzyme powder.
I had sold a co-ownership in him before the disorder developed, and he was
killed in a car crash before many years of treatment and follow-up would
have been completed. Some other fanciers 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 severe or a mild case or is 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 that it is good for various
unspecified causes of diarrhoea, 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 diarrhoea.
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.”
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Canine Digestive Tract Disorders
Polyps
Megaesophagus Torsion Bloat (Volvulus)
Pancreatic
Insufficiency part 3
Fred
Lanting
Continued from Part 2
OTHER DISORDERS
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 Dog seems to
experience a relatively high incidence of this disorder and I believe there
is a genetic propensity, a familial trait, in certain bloodlines.
Diarrhoea and soft stool
Diarrhoea 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. Diarrhoea 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 diarrhoea
are: pancreatic insufficiency, chemical or mechanical irritation of intestinal
linings, parasites, micro organisms, 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 fibre 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 diarrhoea, rush to your veterinary clinic with
the pup and the stool samples. Most of the time the cause of diarrhoea 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 diarrhoea,
and most labs would have no trouble identifying this infection. Generally,
watery diarrhoea is not an indicator of “campy”, but more often has a different
cause. Erythromycin antibiotic is 90% effective against that organism, although
resistant strains may be evolving.
Giardia
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 diarrhoea with a uniquely acrid
“bloody” odour, that experienced breeders can identify quite easily even
before a stool sample is analysed. 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
faeces 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 faeces) and if administered “for 3
days, effectively removes giardia cysts from faeces 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. I prefer the use of Albon™ to control concomitant
bacterial infections in weakened pups, with or without Flagyl for the protozoa,
as mentioned below.
Panacur (fenbendazole) is relatively pricey and seems to be sold only
in large volume jars from the usual vet supply catalogues. For giardia,
Panacur is considered a static drug, 100% effective in clearing cysts from
faeces 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 sulpha 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. Dr. Chuck Kruger,
a Corgi and GSD breeder in Washington State, has been an intensive observer
of this syndrome. Chronic intestinal disease, called overgrowth of intestinal
bacteria in the UK, and probably the same thing that Kruger dubbed “toxic
gut syndrome”, is also being studied in Britain, and has been found to be
a particular problem in younger dogs. Treatment with high dosage of antibiotics
over a long term has been claimed to have a good success rate there. Kruger
pioneered much work in the problem because of so much found in certain American
GSD lines. See http://www.dockruger.com
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 apparently
increases growth of bacteria that are always present there. These Clostridium
and E. coli 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,
yoghurt, 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.
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 seems to 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.
Ulcers
Ulcers have been diagnosed all 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
line bred German Shepherd Dogs with “American lines”. Eosinophilic ulcerative
colitis syndrome is most common in Cocker Spaniels and German Shepherd Dogs.
If your pup or adult has intermittent to constant diarrhoea, 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,
blood-filled balls hanging on the lining of the rectum. 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. They are similar to haemorrhoids in humans in that respect.
END
Fred Lanting is an internationally respected show judge, approved
by many registries as an all breed judge, has judged numerous countries’
Sieger Shows and Landesgruppen events, and has many years experience with
SV. He presents seminars and consults world wide on such topics as Gait
& Structure, HD and Other Orthopaedic Disorders, Anatomy, Training Techniques,
and The GSD. Fred lives part of the year in Alabama, actively trains in
schutzhund, and breeds for occasional litters. He invites all to join his
annual non profit Sieger Show and sightseeing tour.
All Things Canine -- consulting division, Willow Wood Services Phone:
256-498-3319 Fax: 256-498-3311
COPYRIGHT
© Fred Lanting
Reprinted with kind permission of Fred Lanting Author of The Total German Shepherd
Dog and Orthopaedic Disorders
This is
the expanded and enlarged second edition, a "must" for every true GSD
lover. It is an excellent alternative to the "genetic history" by Willis,
but less technical and therefore suitable for the novice, yet very detailed
to be indispensable for the reputable GSD breeder. Chapters include: History
and Origins, Modern Bloodlines, The Standard, Anatomy, The German Shepherd
in Motion, Shows, Showing, and Training, The Winners, Nutrition and Feeding,
General Care and Information, Health and First Aid, Parasites and Immunity,
Diseases and Disorders, The Geriatric German Shepherd, Breeding, Basics
of Genetics, Reproduction, Whelping, The First Three Weeks, Four to Twelve
Weeks, Trouble-shooting Guide
