Inherited gastrointestinal disorders

Portosystemic shunt

roblib — Tue, 30 Mar 2010 15:51:27 +0000

What is ... ?:

Portosystemic shunt (PSS) is a birth defect of the circulation in the liver. In animals with a PSS, there is abnormal blood flow through the liver. Blood should flow from the digestive tract (stomach, intestines) to the liver via the portal system into the blood vessels of the liver, and then to the caudal vena cava which is the large blood vessel carrying blood back to the heart. This way, blood normally percolates through the liver where it is detoxified. In a portosystemic shunt, as the name implies, an accidental shortcut is created: portal blood bypasses the liver and goes directly to the systemic venous circulation (caudal vena cava), without having filtered through the liver tissue. This has very important repercussions because one of the main functions of the liver is to eliminate toxins from the bloodstream. In PSS, blood bypasses the liver and therefore these toxins are not cleared, remaining in the circulation throughout the body. The result is symptoms of PSS, many of which are neurological because the toxins alter the brain's capacity to maintain a dog alert and responsive. The complex of neurological and behavioural signs caused by liver dysfunction is called hepatic encephalopathy.

Portosystemic shunts may occur as intra-hepatic or extra-hepatic depending on the location of the blood vessel in relation to the liver. That is, intrahepatic PSSs are malformations within the liver, whereas extrahepatic PSSs are malformations just upstream from the liver. The location of a PSS is important because it determines the best way to correct it via surgery.

Most animals with congenital portosystemic shunts show symptoms before 6 months of age. When symptoms are subtle, however, the condition may not be diagnosed until much later.

How is ... inherited?:

The exact mode of inheritance is not known, but a genetic basis is clearly indicated by higher-than-average occurrence in certain breeds (see below).

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

The symptoms of PSS tend to emerge during puppyhood. These symptoms generally are associated with the central nervous system, the gastrointestinal tract, or the urinary tract. Most consistently, there are signs of hepatic encephalopathy - neurological and behavioural evidence of diffuse brain dysfunction due to liver dysfunction. Examples include loss of appetite, mental dullness, lethargy and sluggishness, weakness, poor balance, disorientation, blindness, seizures, and even coma. The symptoms may wax and wane, and may worsen after eating a protein-rich meal.

With PSS, a pup's growth may seem to be stunted or slower than the growth of littermates and age-mates. Indeed, "runts" of litters often turn out to be puppies that have birth defects, and PSS is a very common one of these.
Failure of the liver to clear ammonia means that there will be increased excretion in the urine. This commonly leads to urolithiasis - kidney, bladder, or urethral calculi (stones) due to the build-up of mineral salts. Any young dog with urolithiasis (stones in the bladder, urethra, or kidneys) should be checked for PSS.

The first sign of PSS in a dog may be a prolonged recovery from anesthesia, or excessive sedation after treatment with some medications. This occurs because with PSS, anesthetics and medications are not filtered out of the blood and broken down as they would normally be by the liver, but instead are recirculated in the body.
The impact of PSS may not be apparent at first. Symptoms tend to worsen with age, and the decision to treat (via surgery) should be made as early as possible. Dogs do not outgrow PSS; surgery should be performed when a puppy is still growing, to minimize the risk of permanent damage. Dogs who are not candidates for surgery, either because they have a form of PSS that is inoperable or because surgery is not an option due to cost or availability, may still benefit from orally-administered medications at home.
It is very important to realize that the final result of surgery for PSS can only be known weeks after the surgery has been done. The effects of PSS take time to subside, and the body's ability to adapt back to normal after the surgical correction is different in every dog: many become totally normal and have normal lives, whereas some have irreversible damage associated with the PSS, and surgery only partially corrects these changes.

How is ... diagnosed?:

Generally, the diagnosis of PSS is suspected based on a combination of the medical history (such as delayed anesthetic recovery or previous surgery for urolith/urinary tract stone removal), symptoms (such as those described above), and results of laboratory tests. The screening test of choice is a routine laboratory panel (complete blood count, serum biochemistry profile, and urinalysis) with serum bile acids, which is a specific blood test that requires a 12-hour fasting period beforehand and takes 2-3 hours.
The confirmatory test of choice is a high-detail abdominal ultrasound examination by a specialist (radiologist or internist); nuclear scintigraphy (a type of scan) also is highly definitive but is less widely available. Either test is noninvasive and is generally done without sedation.

The screening blood test, serum bile acids, is highly accurate, with a nearly 100% ability to detect PSS in dogs that have it. A positive test still requires ultrasound/scan confirmation, because other disorders such as hepatic microvascular dysplasia, which is an incurable, microscopic version of PSS where thousands of small shunts ("shortcuts") cause blood to bypass the liver at the tissue level, may be present instead. Hepatic microvascular dysplasia can only be confirmed with a liver biopsy, so it is routine for dogs that undergo surgery for PSS to also have a liver biopsy, for identifying whether hepatic microvascular dysplasia is also present. This alters the long-term outlook: dogs with PSS but without microvascular dysplasia have a better long-term outlook for living free of symptoms and without medications.

How is ... treated?:

The most definitive way to deal with PSS is surgery. The surgeon identifies the path of blood bypassing the liver and closes it, forcing the blood to follow the new, normal course through the liver. This type of surgery is an open-abdominal procedure, meaning general anesthesia is warranted and a period of recovery, typically lasting 1-4 days in the hospital and 2 weeks or so at home, is to be expected. The success rate of surgery is high (>90%) but not perfect; even in the most experienced hands, some dogs with PSS who also have microvascular dysplasia or other circulatory defect through the liver may not tolerate the operation and may need only partial closure of the shunt. Other dogs do not tolerate any correction of PSS and this is only apparent during the operation. To improve the chances of success, surgeons often repair PSS by inserting a device that closes the PSS gradually, over several weeks. Surgeons also will be careful to monitor a dog's status both before the surgery and during the post-operative period; the liver performs so many essential functions that careful monitoring and medical support, such as with plasma transfusions, antibiotics, or other treatments, are essential.
In some cases, PSS may involve a single shunt that is buried deep within the liver tissue: intra-hepatic PSS. These situations are difficult to correct in the manner described above, and a better option in such cases is minimally-invasive occlusion (closure) of the shunt through catheter-based techniques. Briefly, this approach does not involve surgical opening of the abdomen but rather involves a surgeon placing a catheter through a blood vessel in the groin and steering the catheter to the location of the shunt within the liver under fluoroscopic, real-time X-ray guidance. The surgeon can then deploy a device that occludes (blocks) blood flow at that level, redirecting it into the normal path. This is an extremely challenging procedure performed only at certain specialist referral hospitals; discussing this possibility with a general practitioner veterinarians is the first step, followed by referral if the features of the PSS are compatible with this procedure.
Finally, many dogs with very mild or no symptoms of PSS, especially if the condition is first identified after 5 years of age, may do well simply by receving oral medications and no surgery at all. To be clear, definitive (surgical) correction is the best treatment, but if the PSS is very minor and it escapes notice until age 5 years or thereafter, there may be more to be gained with a conservative approach and no surgery.

For the veterinarian:

COMPLETE BLOOD COUNT: often unremarkable. Subtle but important clues may include microcytosis, target cells, and/or a mild nonregenerative anemia.
BIOCHEMISTRY: mild abnormalities suggestive of hepatic dysfunction often are present, such as hypoproteinemia, hypoalbuminemia, hypoglycemia, low blood urea nitrogen, and normal to mild increases in serum liver enzymes. Elevated bilirubin levels are inconsistent with PSS and, if repeatable, suggest a different diagnosis. Postprandial serum bile acids (SBA) are consistently elevated (>99% sensitivity for PSS when >25 uM/l).
URINALYSIS: dogs with polyuria and polydipsia often are isosthenuric or hyposthenuric. Ammonium biurate crystals in the urine sediment are an important and common finding. Where urolithiasis occurs, there may also be hematuria, proteinuria, and/or pyuria.
PLAIN RADIOGRAPHY: microhepatica is common.
ADDITIONAL IMAGING TECHNIQUES: ultrasonography, rectal portal scintigraphy, and mesenteric portography (less commonly needed nowadays) can provide information about the presence, location, and type of shunt.

Breeding advice:

Affected individuals and their parents should not be used for breeding. Siblings should only be used after careful screening. If any affected offspring are born, breeding of the parents should be discontinued.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Hart Jr, JR. Portosystemic shunt. In Cote E, ed. Clinical Veterinary Advisor: Dogs and Cats, 2nd ed (St. Louis, MO: Mosby Elsevier, 2011) pp. 905-907.
Berent AC, Weisse C. Hepatic vascular anomalies. In Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine, 7th ed (St. Louis, MO: Saunders Elsevier, 2010) pp. 1649-1672.

Chronic hepatitis

roblib — Wed, 14 Apr 2010 17:23:36 +0000

What is ... ?:

Chronic hepatitis is a catch-all diagnosis for a number of diseases where there is inflammation and death of liver tissue. Affected dogs develop a slowly progressive liver disease. There are many possible causes including viruses, bacterial infection, and some drugs. A familial predisposition to the development of chronic hepatitis exists in some breeds, although the cause is unclear. These breeds are listed below.

In Bedlington terriers and West Highland white terriers, an inherited defect in the metabolism of copper is known to cause chronic hepatitis (copper-associated hepatitis/copper toxicosis in Bedlington terriers). It is estimated that 25% of Bedlington terriers have the disorder, and 50% are carriers (ie. they will not become ill, but can transmit the disorder to their offspring). Copper accumulation occurs in some other breeds as well, but whether the excess in copper is the cause or the result of liver disease is unknown.

How is ... inherited?:

Inheritance in the Bedlington terrier is autosomal recessive. The mode of inheritance is unknown in other breeds.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

The liver has a large reserve capacity, meaning there must be damage to a significant portion before you will see any signs of illness in your dog. The first signs of liver disease are generally vague and non-specific, and include loss of appetite, vomiting, weight loss, depression, lethargy, and/or increased drinking and urination. As the disease becomes advanced, there will be signs more specific to liver failure such as jaundice (you may see yellowing of your dog's eyes for example), coagulation problems, fluid accumulation (ascites), extreme weight loss, and neurologic abnormalities (hepatic encephalopathy) such as head pressing or behavioural changes, due to the build-up of toxins normally metabolized by the liver.

In affected Bedlington terriers, there is progressive accumulation of copper in the liver over time. Associated liver disease may manifest itself in 3 ways.
1) Young dogs (less than 6 years of age) may suddenly develop signs of liver failure, including vomiting, depression and lethargy. Most will die within a few days despite intensive therapy. Others will recover over a few weeks, and thereafter experience occasional milder bouts that may be associated with stressful events such as showing or travelling.
2) In middle-aged to older dogs, similar but less severe signs develop insidiously and the disease has a more chronic course. Gradual weight loss and deterioration in condition are common initially, while specific signs of liver disease (as listed above) develop in the advanced stages of the disease.
3) Young as yet clinically unaffected dogs may be found to have elevated liver copper and biochemical/pathological changes associated with liver disease. These are the dogs in whom treatment will be most effective.
West Highland white terriers are also affected by a disorder of copper accumulation, but the magnitude of increase is less. Diagnosis, signs of illness, and principles of treatment are similar to the Bedlington terrier.

How is ... diagnosed?:

Before liver disease reaches an advanced stage, the clinical signs are generally vague and non-specific. Your veterinarian will do some routine diagnostic blood tests which will show elevations in liver enzymes. This is investigated further with specific liver function tests. Once the problem has been pin-pointed to the liver, your veterinarian will take a liver biopsy which will be sent to a veterinary pathologist. This is necessary to differentiate chronic hepatitis from other causes of liver disease (such as liver cancer or an infection), and to determine the severity and extent of the problem.

How is ... treated?:

Unfortunately, liver damage is often advanced by the time the disease is recognized. Depending on the stage of your dog's illness when it is diagnosed, treatment may involve intravenous fluids, antibiotics, corticosteroids, dietary management, and possibly medication to reduce copper levels in the liver. Your veterinarian will discuss with you the prognosis for your dog.

In Bedlington terriers, there are a few different drugs to control copper accumulation in the liver. These must be given for the life of the dog to prevent further build-up of copper. If the disorder is detected early, when there are no or few clinical signs, these drugs will allow many dogs to live out a normal life.
For the veterinarian: In Bedlington terriers, D-penicillamine (copper chelator which promotes urinary copper excretion), trientine hydrochloride (an alternative copper chelator) or zinc therapy (decreases intestinal copper absorption) may be used to gradually reduce hepatic copper content and prevent further accumulation. Treatment is similar in the West Highland white terrier. Because copper accumulation is not continuous throughout life in the Westie, mature dogs may not require chelation therapy, depending upon hepatic copper levels.
Unfortunately, hepatic liver damage is generally advanced by the time a liver biopsy is taken and the disease is recognized, leading to a poor prognosis. Improvement may occur with prednisone therapy. The usefulness of copper chelation therapy in breeds other than the Bedlington and West Highland white terrier remains unclear.

For the veterinarian:

Elevated ALT is the most consistent biochemical abnormality. With acute onset hepatic necrosis there may be hepatomegaly. With chronic advanced disease, the liver is small and not palpable due to fibrosis and cirrhosis.

Liver biopsy is required for definitive diagnosis of chronic hepatitis, to characterize the extent of fibrosis and progression to cirrhosis (which is by definition irreversible and indicatative of a poor long-term prognosis), and also to quantify hepatic copper levels. The key histopathologic feature is moderate to severe inflammation. The role of hepatic copper accumulation is controversial. Copper is commonly elevated, but this is believed by most to be secondary to the chronic inflammation, in contrast to the primary copper accumulation that causes copper-associated hepatitis in Bedlington and West Highland white terriers.
Copper-associated hepatitis should be suspected in any Bedlington terrier with physical or biochemical evidence of liver disease, and biochemical screening should be done in any Bedlington terrier with a vague illness. Asymptomatic affected dogs can be detected through biochemical screening (2/3 will have elevated ALT), liver biopsy, or a radioisotope study using copper-64. Affected dogs will have reduced stool radioactivity compared with normal dogs, due to reduced biliary excretion of copper. A genetic marker has been identified for copper toxicosis in Bedlington terriers that will detect affected and carrier dogs at any age - see www.vetgen.com

Breeding advice:

A genetic marker has been identified for copper toxicosis in Bedlington terriers that will detect affected and carrier dogs at any age - (see www.labvetgen.ca or www.vetgen.com) Because of the prevalence of this serious disorder in the Bedlington terrier, all dogs to be used for breeding should be tested. The results may be registered wth the Orthopedic Foundation for Animals (see www.offa.org) Testing may also be done by liver biopsy but dogs must be older than 1 year of age so that sufficient copper accumulation will have occurred to be detectable.

There is no similar testing available for other breeds. Affected dogs should not be bred, and breeding of their parents should be avoided as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Johnson, SE.1995. Diseases of the liver. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, pp. 1313-1357. W.B. Saunders Co., Toronto.

Leveille-Webster, C.R. and Center, S.A. 1995. Chronic hepatitis: therapeutic considerations. In J.D. Bonaguara and R.W. Kirk (eds.) Kirk's Current Veterinary Therapy XII Small Animal Practice. pp. 749-756. W.B. Saunders Co., Toronto.
Twedt, D.C. 1997. Treatment of chronic hepatitis. ACVIM- Proceedings of the 15th Annual Vet. Med. Forum, pp.234-236.

Leveille-Webster, C.R. 1996. Medical management of inflammatory hepatic disease in dogs. ACVIM-Proceedings of the 14th Annual Vet. Med. Forum, pp. 43-44.

Orthopedic Foundation for Animals, Registry for Copper Toxicosis in Bedlington Terriers, www.offa.org

Cleft lip/palate

roblib — Wed, 14 Apr 2010 17:36:34 +0000

What is ... ?:

This is an opening in the lip or the roof of the mouth that occurs due to failure of normal fusion processes during embryonic development. Cleft palate and cleft lip may result from either hereditary or environmental causes (such as the use of certain drugs during pregnancy).

How is ... inherited?:

Cleft palate is believed to be an autosomal recessive trait in the Brittany spaniel. In the English and French bulldog, pointer, and shih tzu, the trait may be autosomal dominant with incomplete penetrance.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

Affected pups are born with the condition. A minor defect will cause little or no problem, while a more severe defect will cause signs such as a chronic nasal discharge (that may include food), poor growth, aspiration pneumonia (from inhalation of food), or even death.

How is ... diagnosed?:

Your veterinarian will diagnose these conditions on physical examination.

How is ... treated?:

Mild problems may not require any treatment, but more serious defects will require surgical repair to prevent complications such as aspiration pneumonia.

Breeding advice:

Affected animals should not be used for breeding, and it is prudent to avoid breeding their parents and siblings as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Gastric dilatation-volvulus

roblib — Thu, 15 Apr 2010 17:50:47 +0000

What is ... ?:

Gastric dilatation-volvulus (GDV) is a very serious condition that occurs in susceptible dogs when the stomach becomes distended with air, and then while dilated, twists on itself. This interferes with the blood supply to the stomach and other digestive organs, and blocks the passage of food, leading to worse bloat. The distended stomach impedes the normal return of blood to the heart, causing drastically reduced cardiac output and a decrease in blood pressure. Blood/oxygen-deprived tissues start to die, releasing toxins into the blood stream which among other adverse effects, cause serious disturbances in heart rhythms (cardiac arrhythmias) - a common cause of death in these dogs.

Simple gastric dilatation does not produce volvulus (twisting) in an otherwise normal stomach. Dogs most susceptible to GDV are the large, deep-chested breeds, in whom the stomach appears to be more mobile within the abdomen. Other factors that increase the risk for GDV include overeating, rapid eating, single daily feeding, high water consumption, stress, and exercise after eating.

How is ... inherited?:

It appears that conformation and size are what predispose a particular breed to this disorder, such that breeds with a deeper and narrower chest are most susceptible. Within such a breed, dogs with a higher thoracic depth/width ratio (ie. the deepest, narrowest chests) are the most vulnerable to GDV.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

GDV is one of those thankfully rare conditions in which your dog can go from being healthy to critically ill over the course of a few hours. Even with appropriate veterinary care, approximately one third of dogs with this condition will die.

Initiation of GDV occurs when a susceptible dog swallows air while gulping food or water, possibly in association with exercise. You will first notice that your dog is uncomfortable - pacing, restless - and appears bloated. There may be unproductive retching/vomiting. Discomfort progresses to depression and if the dog does not receive treatment, to coma and death. This can all happen within 6 hours or less.

How is ... diagnosed?:

GDV must be diagnosed and treatment initiated quickly if your dog is to survive. The condition is usually readily diagnosed on physical examination.

How is ... treated?:

The two urgent priorities are to remove the gas from the stomach (via stomach tube) and start treatment for shock. Your veterinarian will then perform surgery to reposition the stomach, assess the extent of damage, and do a gastropexy to anchor the stomach to the abdominal wall and prevent recurrence of GDV.

Intensive care is required in the immediate post-operative period when dogs may face a number of life-threatening problems including shock, electrolyte imbalance, cardiac arrhythmias, and wide-spread infection (septicemia).
Prevention: There are some simple things you can do to reduce the chance of bloat, if you have a dog of a susceptible breed. Basically, you want to avoid your dog consuming a large amount of food or water all at once, especially not at the same time as vigorous exercise. Rather than feeding once a day or leaving food always available, feed in divided portions. Have fresh clean water always accessible but take it up at mealtimes (so your dog doesn't gulp it with food). Avoid exercising your dog before and after meal times.

Breeding advice:

It may be possible to reduce the incidence of GDV in susceptible breeds by selectively breeding dogs with lower thoracic depth/width ratios.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Glickman, L.T., Glickman, N.W., Perez, C.M., et. al. 1994. Analysis of risk factors of gastric dilitation and dilitation-volvulus in dogs. J. Am. Vet. Med. Assoc. vol 24: 1465-1471.

Schaible, R.H., Ziech, J., Glickman, N.W., et. al. 1997. Predisposition to gastric dilitation volvulus in relation to genetics of thoracic conformation in Irish setters. J. Am. Animal Hosp. Assc. vol 33:379-383.

Gluten-sensitive enteropathy

roblib — Thu, 15 Apr 2010 18:05:38 +0000

What is ... ?:

This is a disorder of the small intestine that results from a sensitivity or intolerance to gluten, the protein part of wheat. There are many similarities to celiac disease in people, although the intestinal damage and clinical signs are less severe in dogs. Gluten-sensitve enteropathy is controlled by feeding a gluten-free diet.

How is ... inherited?:

unknown

What breeds are affected by ... ?:

Irish setter

What does ... mean to your dog & you?:

Signs of this disorder are usually apparent by about 6 months of age. Affected dogs fail to gain weight normally or start losing weight, and most develop chronic diarrhea.

How is ... diagnosed?:

There are various blood and fecal tests that will point your veterinarian to a diagnosis of gluten-sensitive enteropathy as a cause of your dog's diarrhea. The diagnosis is confirmed if the clinical problems resolve following the introduction of a gluten-free diet.

How is ... treated?:

This disorder is treated by feeding a nutritionally balanced gluten-free diet to your dog for life. Typically the signs resolve within 4 to 6 weeks of the diet change.

For the veterinarian:

Low serum folate and reduced xylose absorption are indirect evidence of proximal small bowel disease. Serum cobalamin and duodenal juice culture are generally normal. Jejunal biopsies show partial villous atrophy, typically by 4 months of age.

Breeding advice:

Affected dogs should not be bred and until more is known about inheritance of this disorder, it is prudent to avoid breeding their parents and siblings as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Histiocytic ulcerative colitis

roblib — Thu, 15 Apr 2010 18:57:10 +0000

What is ... ?:

Colitis means inflammation of the large intestine. Histiocytic colitis is one form of inflammatory bowel disease (IBD), in this case associated with infiltration of inflammatory cells (histiocytes) into the intestinal wall which is thought to be due to a defect in immune regulation. The result is chronic large bowel diarrhea.

This disorder has some similarities to Crohn's disease in people.

How is ... inherited?:

unknown

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

This condition generally develops in young dogs (less than 1 year). Because this is a problem in the large intestine, your dog will have signs such as an increased frequency of passing stool (although the volume may be normal), straining to defecate, and the presence of blood or mucous in the stool. There is usually an increased sense of urgency for your dog, which often means "accidents" in the house. There may be intermittent vomiting, lethargy, loss of appetite and weight loss.

How is ... diagnosed?:

There are many disorders that cause chronic diarrhea in dogs, so diagnosis is not simple. Your answers to questions about frequency and appearance of the increased stool will help point your veterinarian towards large bowel disease. S/he will do blood and fecal tests for parasites, bacterial infections and other possible causes. An intestinal biopsy is necessary for a definitive diagnosis of histiocytic ulcerative colitis. This involves surgical removal of small samples of your dog's intestinal wall for examination by a veterinary pathologist.

How is ... treated?:

This disorder is difficult to control. Treatment consists of dietary management, and immunosuppressive and anti-inflammatory drugs to reduce the intestinal inflammation. The diet should be free of additives and preservatives and contain an adequate (but not excessive) amount of highly digestible protein, with supplementation of fiber. Your veterinarian will recommend an appropriate commercial diet or provide a recipe for a homemade diet that meets these requirements.

For the veterinarian: Treatment is largely empiric. Anti-inflammatory drugs such as corticosteroids, sulfasalazine, and metronidazole are used, often in combination. Other immunosuppressive drugs may be tried if prednisone fails. Newer drugs are also being tried for treatment of Crohn's disease in people, that may prove useful in dogs.

For the veterinarian:

Colonoscopy may show evidence of the disease (increased mucosal granularity, friability and diffuse erosions) but histopathology is necessary for a definitive diagnosis, and will show a mixed inflammatory cellular infiltrate with PAS-positive histiocytes.

Breeding advice:

Affected dogs should not be bred and until more is known about inheritance of this disorder, it is prudent to avoid breeding their parents and siblings as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Dimski, D.S. 1995. Therapy of inflammatory bowel disease. In J.D. Bonagura and R.W. Kirk (eds.) Kirk's Current Vet. Therapy XII Small Animal Practice. pp. 723-728. W.B. Saunders Co., Toronto.

Jergens, A.E. and Willard, M.D. 2000. Diseases of the large intestine. In E.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, Chapter 138. W.B. Saunders Co., Toronto.

Hyperlipoproteinemia

roblib — Thu, 15 Apr 2010 19:08:40 +0000

What is ... ?:

In this disorder there is an excess of fats and fat-like substances (lipoproteins) in the blood, resulting from a defect in lipoprotein metabolism. The two clinically important lipids in dogs are cholesterol and triglycerides. There are similarities to familial hypertriglyceridemia in people.

How is ... inherited?:

The mode of inheritance is unknown.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

An elevation of triglycerides (hypertriglyceridemia) usually causes periodic episodes of vomiting and diarrhea with abdominal discomfort and lack of appetite. These signs last for a few hours or days and may resolve on their own while your dog doesn't eat.

Sustained high blood levels of glycerides are also associated with an increased risk for pancreatitis, a life-threatening disease which causes profuse vomiting and severe abdominal pain.
Elevated blood cholesterol levels on their own do not appear to cause any problems.

How is ... diagnosed?:

Your veterinarian will likely suspect this condition based on clinical signs (described above) together with a fatty (lipemic) blood sample. Although it is not uncommon for any dog to have fat in a blood sample shortly after a meal, a sample that is lipemic after 12 hours of fasting is diagnostic for high blood levels of triglycerides.

Sometimes hypertriglyceridemia only becomes apparent when your veterinarian takes a blood sample from your dog for an unrelated reason.
Hypercholesteremia on its own doesn't cause clinical signs, but may be found incidentally on a blood sample.

How is ... treated?:

Restriction of dietary fat is the most important therapy for hypertriglyceridemia. Once a diet has been established that will keep the level of triglycerides in the blood below a certain level, your dog will need to stick to the diet for life. Your veterinarian will monitor the levels of triglycerides annually or if there is an unexplained episode of vomiting and diarrhea.

It is important for you or anyone caring for your dog to be aware of the risks of consuming a large amount of fat in a single meal ( eg. garbage) which can bring on a fatal episode of pancreatitis.
Due to the risks associated with sustained high blood levels of triglycerides, even dogs without clinical problems at the time of diagnosis should undergo dietary management to restrict fat.
Treatment is not required for hypercholesteremia.
For the veterinarian: The goal is to achieve, with dietary management, a serum TG (in uncleared serum) of 500 mg/dl and a normal CH, with little or no weight loss. There are some drug therapies that have been tried but the benefits have not been substantiated.

For the veterinarian:

Normal post-prandial dogs may have a transient (6 - 10 hours), modest (150 - 400 mg/dl) elevation of serum triglycerides. A grossly lipemic fasting serum sample is diagnostic for hypertriglyceridemia. Hypercholesterolemia can only be detected by laboratory examination.

Hyperlipidemia is clinically important when fasting triglyceride concentrations exceed 500 mg/dl or cholesterol exceeds 300 mg/dl. It is important that the values be measured on uncleared serum samples.

Breeding advice:

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Ford, R.B. 1995. Canine hyperlipidemia. in S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, pp.1414-1419. W.B. Saunders, Toronto.

Immunoproliferative (Basenji) enteropathy/lymphocytic-plasmacytic enteritis

roblib — Fri, 16 Apr 2010 16:56:02 +0000

What is ... ?:

Inflammatory bowel disease is a common cause of chronic diarrhea and vomiting in the dog. The lining of the stomach or small or large intestine becomes infiltrated with inflammatory cells, and this interferes with the normal functions of digestion and absorption. This immune-related inflammation may be a response to parasites, bacterial infection, dietary sensitivities, or intestinal cancer, but in most cases, no obvious cause is found.

In the Basenji, a hereditary lymphocytic-plasmacytic enteritis has been identified, called immunoproliferative enteropathy, which causes severe intestinal malabsorption and loss of protein (protein-losing enteropathy).

How is ... inherited?:

unknown.

What breeds are affected by ... ?:

Basenji

What does ... mean to your dog & you?:

This condition is usually first seen in young adult (to middle-aged) Basenjis. There are intermittent bouts of severe diarrhea which may be preceded by loss of appetite, and may be associated with stressful events such as boarding, travel, or vaccination. Weight loss is common, due to loss of protein and other nutrients from the gut. Without treatment, the conditon becomes progressively worse leading to emaciation.

How is ... diagnosed?:

There are many disorders that cause intermittent diarrhea in dogs, so diagnosis is not simple. Your veterinarian will do blood and fecal tests for parasites, bacterial infections and other causes of diarrhea. An intestinal biopsy is necessary for a definitive diagnosis of this condition. This involves surgical removal of small samples of your dog's intestinal wall for examination by a veterinary pathologist.

How is ... treated?:

There is no cure for this condition, but it can often be controlled if treatment is started early. Dietary management is important, using a special intestinal diet with a good quality protein source and without additives. Because it is the hyperactive immune response that leads to tissue damage and interferes with normal intestinal function, treatment is aimed at suppressing that response and decreasing the inflammation present in the gastrointestinal tract. Corticosteroids (prednisone) are used for this purpose, starting at a relatively high dose. Usually your dog's condition will begin to improve in 1 or 2 weeks and after 1 or 2 months, your veterinarian will begin to gradually reduce the dose to alternate day therapy.

Side effects of corticosteroid treatment include an increase in drinking and appetite, and weight gain. These are less of a problem at low doses. There are other immunosuppressive drugs that may be used in combination with corticosteroids, if the response to the latter is unsatisfactory or the side effects are unacceptable.

For the veterinarian:

Hypergammaglobulinemia is seen with this condition. Endoscopy may reveal normal- or abnormal-looking GI mucosa. A full-thickness biopsy (surgical or by endoscopy) is essential for definitive diagnosis.

Since the primary treatment for inflammatory bowel disease is immunosuppression, it is imperative to rule out possible infectious causes of GI disease such as Giardia, Salmonella, histoplasmosis, intestinal bacterial overgrowth, etc.

Breeding advice:

Affected dogs should not be bred and, until more is known about the mode of inheritance, it is preferable to avoid breeding their parents and siblings as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Burrows, C.F., Batt, R.M., Sherding, R.G. 1995. Diseases of the small intestine. In E.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, pp. 1169-1232. W.B. Saunders Co., Toronto.

Ackerman, L. 1999. The Genetic Connection: A Guide to Health Problems in Purebred Dogs. p. 77. AAHA Press, Lakewood, Colorado.

Intestinal lymphangiectasia

roblib — Fri, 16 Apr 2010 17:03:58 +0000

What is ... ?:

As part of the normal circulatory system, lymph fluid is collected from tissues throughout the body and returned to the blood by way of the lymphatic vessels. In intestinal lymphangiectasia, normal drainage is blocked so that intestinal lymph leaks into the intestines instead of being returned to the circulation. This results in the loss of proteins, lymphocytes ( a type of white blood cell), and lipids or fats into the stool.

Intestinal lymphangiectasia may be congenital (present from birth) due to malformation of the lymphatic system, or it may be acquired in association with another disease.

How is ... inherited?:

The inheritance is not known.

What does ... mean to your dog & you?:

Signs of intestinal lymphangiectasia usually develop slowly over several months, and may come and go. Your dog may fail to gain weight or may progressively lose weight. The loss of protein into the bowel causes loss of fluid from the circulation into the limbs, the abdomen, or the chest. Your dog's legs and/or abdomen may appear swollen and he/she may have trouble breathing. There may be a chronic persistent or intermittent diarrhea due to the loss of protein, fluid and fat into the bowel.

How is ... diagnosed?:

If your dog has the signs described above, your veterinarian will likely suspect one of the diseases that result in loss of proteins into the gut. Laboratory tests and an intestinal biopsy are necessary to diagnose the specific cause.

How is ... treated?:

This condition can not be cured but it can generally be well-managed by you and your veterinarian. Remissions of several months with occasional flare-ups are common.
The major goal of therapy is to reduce the loss of proteins into the intestine, to restore normal protein levels in your dog. This is done through diet, and medication to reduce inflammation in the intestinal wall. An ideal diet for dogs with intestinal lymphangiectasia contains minimal fat, and an ample quantity of high-quality protein. There are commercial prescription diets available which fulfill these requirements, or your veterinarian can give you information to prepare a low-fat diet at home. In either case, you will need to supplement your dog's diet with fat-soluble vitamins, due to the poor absorption of fat that occurs with this condition.

Corticosteroids are given to reduce inflammation, and thereby reduce loss of protein and associated diarrhea. Your veterinarian may also prescribe antibiotics.

For the veterinarian:

CLINICAL: diarrhea is usually mild or inapparent, in comparison with other protein-losing enteropathies.

LABORATORY: hypoproteinemia with hypocholesteremia, lymphocytopenia, and/or hypoglobulinemia; frequently also see hypocalcemia due to vitamin D and calcium mal-absorption. It is important to assess liver and kidney function to rule out non-enteric causes of hypoproteinemia.
SURGERY: a biopsy is necessary for definitive diagnosis by histologic examination. At surgery, usually see prominent network of milky distended lymphatic channels in the mesentery or on serosal surface.

Breeding advice:

Dogs with familial intestinal lymphangiectasia and their close relatives should not be used for breeding.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Burrows, C.F., Batt, R.M., Sherding, R.G. 1995. Diseases of the small intestine. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine. p. 1224-1225. W.B. Saunders Co., Toronto.

Williams, D.A. 1998 Protein-losing enteropathy Proc. 16th ACVIM Forum pp 419-421

Megaesophagus

roblib — Fri, 16 Apr 2010 17:16:23 +0000

What is ... ?:

With this condition, there is dilation of the esophagus due to a loss of normal peristaltic function. Peristalsis is the process by which waves of muscular contraction move along the contents (food in this case) of tubular organs. Animals with megaesophagus regurgitate undigested food shortly after eating.

Dogs may be born with esophagus or they may develop it later in life. It is commonly seen with other disorders such asmyasthenia gravis and peripheral neuropathies

How is ... inherited?:

This is an autosomal recessive trait in the wire-haired fox terrier, and autosomal dominant in the miniature schnauzer. The mode of inheritance has not been determined for other breeds that are predisposed to this condition.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

Although it may not be noticed until young adulthood, this disorder is usually first recognized in puppies around the time of weaning. Affected pups regurgitate food, fail to thrive, and may develop respiratory difficulties associated with aspiration pneumonia due to inhalation of food particles. Signs include laboured breathing, fever and lethargy, and nasal discharge.

Some dogs appear to gradually outgrow this condition (by a year or so), while in others there is no improvement.

How is ... diagnosed?:

Regurgitation of undigested food shortly after eating is the main sign with this disorder. Your veterinarian will take chest x-rays to determine if your dog has megaesophagus, and perform other laboratory tests since there are several conditions that may be associated with this disorder.

How is ... treated?:

If an underlying cause can be identified, treatment may improve esophageal function. There is no specific treatment for the megaesophagus itself, but it can usually be managed by feeding small, frequent, high-caloric meals from an elevated location so that gravity assists the passage of food. Different consistencies of foods can be tried to determine which causes the least regurgitation.

Some dogs appear to outgrow the problem, while in others there is no improvement and feeding management is required for life. Your veterinarian will discuss with you possible complications that you must watch out for, the most serious of which is aspiration pneumonia.

For the veterinarian:

Since megaesophagus may be associated with many different conditions, the diagnostic work-up should include CBC, biochemical profile, urinalysis and survey thoracic radiographs in all cases.

Breeding advice:

Affected wire-haired fox terriers, their parents (carriers of the trait) and siblings (suspect carriers) should not be bred. Affected miniature schnauzers should not be bred.

In other breeds in which inheritance is unknown, it is safest to avoid breeding affected dogs, their parents and siblings.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Twedt, D.C. 1995. Diseases of the esophagus. In E.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine, pp.1124-1142. W.B. Saunders Co., Toronto.

Jenkins, C.C. and Mears, E.A. 1996. What's new in the diagnosis and management of megaesophagus. ACVIM-Proceedings of the 14th Annual Vet. Med. Forum, p. 585-586.

Pancreatitis

roblib — Fri, 16 Apr 2010 17:19:45 +0000

What is ... ?:

Normally, digestive enzymes are produced by the pancreas and secreted into the small intestine where they are essential for the digestion of protein. In pancreatitis these enzymes are activated while still in pancreatic cells, and essentially begin to digest the pancreas itself. This causes the death of pancreatic and surrounding tissue, hemorrhage, acute abdominal pain, and vomiting. The tissue damage becomes self-perpetuating as toxic factors are released into the circulation.

No one specific cause of pancreatitis is known, but several associated factors have been identified. These include high levels of fats in the blood (hyperlipoproteinemia), certain drugs, disruption to the blood supply to the pancreas (during shock for example), some toxins, and certain diseases like diabetes mellitus and hypothyroidism.

How is ... inherited?:

Inheritance has not been established, although certain breeds are clearly predisposed to this disorder.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

Pancreatitis is generally seen in dogs older than 6 years of age. There is usually depression, loss of appetite, vomiting, and sometimes diarrhea. This may occur off and on over several weeks or it may develop very suddenly and dramatically, with severe abdominal pain, vomiting, shock and collapse. The onset of pancreatitis sometimes follows a high-fat meal, if your dog finds an opportunity to feast on garbage for example.

How is ... diagnosed?:

There are many disorders that cause these clinical signs. Your veterinarian will do x-rays and blood tests that will lead to the diagnosis, and also to look for other contributing causes.

How is ... treated?:

Treatment is aimed at maintaining your dog's fluid and electrolyte balance, to treat or prevent shock while the pancreas is "rested" by withholding food, to allow it to recover. Antibiotics and medication to relieve pain are also given. Any contributing factors that can be identified are treated as well, which may require surgery (for example bile duct obstruction or pancreatic abscess).

With treatment, mild cases of pancreatitis usually recover after a few days. Many of these will be fine over the long term, as long as high fat meals are avoided. Other dogs may develop recurring pancreatitis.
Severely affected dogs will require several days of intense therapy, and there may be complications such as bleeding disorders or acute renal failure. Some of these dogs will die despite good supportive care.

For the veterinarian:

The following are commonly seen: leukocytosis, prerenal azotemia, increased liver enzymes, hyperglycemia, hypercholesterolemia and hypertriglyceridemia (often with grossly evident hyperlipidemia), and elevated amylase and lipase. There are some assays available for pancreatic enzymes and zymogens in serum [check with your diagnostic laboratory], and more being developed which may prove to be of practical diagnostic value.

Breeding advice:

Although inheritance has not been proved, it is best not to breed dogs from families where pancreatitis is prevalent. This can be difficult because most cases occur in dogs older than 6 or 7 years of age, who may have been used in breeding programmes already.
FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Perianal fistula

roblib — Fri, 16 Apr 2010 17:33:15 +0000

What is ... ?:

Perianal fistula is a painful, chronic condition in which single or multiple ulcerated tracts develop in the tissue around the anus. No one clear cause has been established, although many have been considered. Some of the factors involved appear to be a broad tail base and low tail carriage, and an increased density of sweat glands in the anal region. It is these sweat glands that become inflamed and infected, leading to the draining sinus tracts typical of this condition.

How is ... inherited?:

unknown, but there is a strong breed predisposition for the breeds mentioned below.

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

This condition is painful for your dog. The types of signs you will see include straining or pain with defecation, bleeding, constipation, fecal incontinence, licking of the area, and malodorous anorectal discharge. These signs worsen as more tissue in the area around the anus becomes affected.

How is ... diagnosed?:

Diagnosis is usually straightforward, based on your description of what you observe in your dog, and on physical examination in which your veterinarian will find single or multiple areas of ulceration and draining tracts, with pus and blood. Your veterinarian may also take a skin biopsy if s/he suspects a tumour in the area (which usually has a more raised appearance, but can also be associated with extensive ulceration).

How is ... treated?:

This is a difficult condition to treat. Medical treatment (combination of antibiotics, antiseptics, and anti-inflammatory drugs) only provides temporary relief, and is usually not successful in clearing up the condition. Generally surgery is required, and there are several methods used including surgical removal of the tracts, freezing or cautery of the tissue, and tail amputation. Possible post-operative complications include significant bleeding, fecal incontinence, and recurrence of the tracts.

In mild cases, surgery often results in complete resolution of the problem, without recurrence. Where the problem is more severe (more tissue destruction), there is a lower rate of success and a higher occurrence of complications. Your veterinarian will discuss all this with you when considering what is best for your dog.

Breeding advice:

Although the inheritance (or even the cause of the condition) is not understood, it is preferable not to breed affected animals.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Protein-losing enteropathy

roblib — Fri, 16 Apr 2010 17:40:07 +0000

What is ... ?:

Excessive loss of plasma and proteins into the gastrointestinal (GI) tract is called protein-losing enteropathy. It can result from any condition that damages the lining of the GI tract. Protein-losing enteropathies that are thought to have an inherited component include intestinal lymhangiectasia, immunoproliferative enteropathy , and protein-losing enteropathy and nephropathy in the soft-coated wheaten terrier. The latter condition is thought to be related to adverse food reactions, and there is also loss of protein from the kidney (see also familial renal disease).

How is ... inherited?:

The inheritance may be autosomal recessive.

What breeds are affected by ... ?:

Soft coated wheaten terrier

What does ... mean to your dog & you?:

Your dog may fail to gain weight or may progressively lose weight. The loss of protein into the bowel causes loss of fluid from the circulation into the limbs, the abdomen, or the chest. Your dog's legs and/or abdomen may appear swollen and he/she may have trouble breathing. There may be a chronic persistent or intermittent diarrhea due to the loss of protein, fluid and fat into the bowel. Loss of protein from the kidney will cause increased urination and drinking in your dog.

How is ... diagnosed?:

How is ... treated?:

This condition can not be cured but it can generally be well-managed by you and your veterinarian. The major goal of therapy is to reduce the loss of proteins into the intestine, to restore normal protein levels in your dog. This is done through diet, and medication to reduce inflammation in the intestinal wall. An ideal diet for dogs with protein-losing enteropathy contains minimal fat, and an ample quantity of high-quality protein. There are commercial prescription diets available which fulfill these requirements, or your veterinarian can give you information to prepare a low-fat diet at home. In either case, you will need to supplement your dog's diet with fat-soluble vitamins, due to the poor absorption of fat that occurs with this condition.

Corticosteroids may help to reduce inflammation, and thereby reduce loss of protein and associated diarrhea.

Breeding advice:

Affected dogs should not be used for breeding. Given that the inheritance is thought to be autosomal recessive, parents (considered carriers) and siblings (suspect carriers) should not be used for breeding either.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Williams, D.A. 1998 Protein-losing enteropathy Proc. 16th ACVIM Forum pp 419-421

Pyloric stenosis

roblib — Fri, 16 Apr 2010 18:09:58 +0000

What is ... ?:

In this condition, there is a narrowing (stenosis) of the pylorus, the region of the stomach through which food and liquid pass into the small intestine. Affected animals vomit after eating. In the congenital form, pups are born with the condition.

How is ... inherited?:

unknown

What breeds are affected by ... ?:

What does ... mean to your dog & you?:

In the congenital form, the condition usually becomes apparent at the time of weaning. The main sign is vomiting which begins with the introduction of solid food to the puppies.

How is ... diagnosed?:

Diagnosis is based on clinical signs and contrast radiography (showing that the stomach does not empty normally), or endoscopic examination.

How is ... treated?:

Very mild cases can be treated by feeding small, frequent, highly digestible meals. Other cases require surgery; most dogs do well post-operatively.

Breeding advice:

Although the mode of inheritance is not known, it is preferable not to breed affected dogs, or their parents or siblings.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Small intestinal bacterial overgrowth (SIBO)

roblib — Fri, 16 Apr 2010 18:13:54 +0000

What is ... ?:

In this condition, there is a dramatic increase in the number of bacteria in the small intestine, and this interferes with normal absorption of nutrients. The result is chronic intermittent diarrhea, and weight loss or failure to gain weight.

In the German shepherd, this condition is thought to be related to a deficiency of immunoglobulin A (IgA) , the primary immune defense in the small intestine.
Small intestinal bacterial overgrowth (SIBO) may develop in association with exocrine pancreatic insufficiency. It may also be seen with inflammatory bowel disease, although it can't always be determined which came first.

How is ... inherited?:

unknown

What breeds are affected by ... ?:

German shepherd

What does ... mean to your dog & you?:

The condition is usually seen in young dogs, who develop chronic intermittent diarrhea which gradually gets worse, and lose weight or fail to gain weight normally. Some dogs may only show weight loss and in others there may be vomiting.

How is ... diagnosed?:

There is no straightforward test to diagnose SIBO. Because the condition may develop as a complication of many intestinal diseases, it is important to search for any possible underlying cause. Your veterinarian will do tests for parasites, bacterial infections, partial obstruction, and other causes of diarrhea such as exocrine pancreatic insufficiency. Besides these baseline blood and fecal tests, there are several other tests that can be done to support the diagnosis of SIBO.

How is ... treated?:

Antibiotics are used at the same time as any underlying cause is treated. Often, no underlying cause can be found and it becomes a question of long term management. The disorder can usually be controlled with long courses of antibiotics, repeated occasionally if there is a relapse, and dietary management using a therapeutic diet low in carbohydrates and fats.

For the veterinarian: Four weeks of treatment with oxytetracyline is usually successful. Some dogs with SIBO relapse soon after antibiotics are discontinued. This may mean there is an unidentified underlying cause, or there has been permanent functional mucosal damage. Antibiotics, gradually reduced to the lowest dose that will control the diarrhea, may need to be continued for extended periods.

For the veterinarian:

Bacterial overgrowth in the proximal small bowel is increasingly recognized as an important cause of chronic intermittent small bowel diarrhea +/- weight loss in many breeds. There is overgrowth of anaerobic bacteria, which have a greater potential for damaging the intestinal mucosa and causing malabsorption. Anaerobes are also the major cause of bile salt deconjugation, the results of which are fat malabsorption and steatorrhea.

There is no straightforward test to diagnose SIBO. Increased serum folate or reduced cobalamin provide indirect support for the diagnosis, once pancreatic insufficiency has been ruled out. Other helpful tests include absorption and permeability tests and hydrogen breath testing (available in some specialty centres). The diagnosis can be confirmed by microbiologic culture of duodenal juices (obtained endoscopically or by laparotomy) although this is expensive and technically complicated, and may miss some cases of SIBO.

Breeding advice:

Affected dogs should not be bred, and until more is known about inheritance of this disorder, it is prudent to avoid breeding their parents and siblings as well.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources:

Rutgers, H.C. 1998. Diagnosis and long-term management of bacterial overgrowth in the dog. ACVIM-Proceedings of the 16th Annual Vet. Med. Forum. pp. 482-484.