Small Intestinal Bacterial Overgrowth

Introduction: Small intestinal bacterial overgrowth (SIBO) is characterized by an uncontrolled increase in the number of bacteria (10⁵ colonies/ml intestinal fluid) in the upper small intestine.  It is considered by some to be an important cause of diarrhea in small animals.  SIBO may occur secondary to a number of other intestinal disorders, or be idiopathic.

Factors which can cause Secondary SIBO include:

• Ileus (impaired GI motility):  Bacterial populations normally increase in number proximally to distally in the GI tract.  Peristalsis is one important mechanism that limits bacterial populations in the upper small intestine by flushing bacteria distally through the GI tract.  Conditions that cause ileus have classically been associated with bacterial overgrowth.  There are many causes of ileus, including intestinal obstruction, neuropathy, abdominal surgery, peritonitis, pancreatitis, uremia, hypokalemia, and endotoxemia.  "Blind loop syndrome" refers to an anatomical out-pouching of gut or a  mesenteric hernia that results in a localized ileus, which may then cause SIBO.

• Increased substrate:  Conditions which result in increased nutrients in the lumen of the bowel can allow bacteria in the small intestine to overgrow by providing substrate.  This occurs with motility disorders, and maldigestive disorders, such as exocrine pancreatic insufficiency (EPI).

• Host malnutrition: A decrease in body condition can have deleterious effects on the local gut immunity and mucus secretion.  This may lead to uncontrolled bacterial proliferation.

Idiopathic SIBO:  Idiopathic SIBO is also referred to as antibiotic-responsive SIBO, and is seen more commonly in young German Shepards than in any other breed.  Animals with idiopathic SIBO will have a decrease in signs following the appropriate antibiotic regimen.

Pathophysiology: There are several mechanisms by which bacterial overgrowth causes clinical signs:

• Bacteria cause deconjugation of bile salts.  These products are then allowed to be reabsorbed from the intestinal lumen, making them unavailable to participate in fat absorption.  This inability to break down and absorb fats causes both an osmotic and a secretory diarrhea since deconjugated bile acids stimulate enterocyte secretion.

• Bacteria cause hydroxylation of fatty acids.  Hydroxylated fatty acids inhibit fluid absorption, and may act synergistically with deconjugated bile acids in stimulating enterocyte secretion.  Fatty acids further damage enterocytes by their detergent properties, which solubilize components of the cell membrane.  This enterocyte damage may result in some degree of villous atrophy, which is sometimes seen in association with SIBO.

• Bacteria change brush border enzyme activity. Increased bacterial populations can also lead to maldigestion by causing changes in the enzyme activity of the brush border cells, and disrupting the mucosal stage of digestion.  This change in the mucosal function is reversible with antibiotic therapy, and does not cause any structural damage that would be evident on histopathology.

• Bacteria compete for nutrients. Excess bacteria compete for nutrients in the lumen of the bowel, resulting in malabsorption and weight loss.

Signalment:

• Idiopathic SIBO:  Young, large-breed dogs and German Shepards seem to be more likely to have idiopathic SIBO.  Idiopathic SIBO is not recognized in cats.  

• Secondary SIBO:  This condition may be seen in all breeds and ages of dogs.

Clinical signs:  

• Idiopathic SIBO:  Dogs with idiopathic SIBO present with chronic intermittent small bowel diarrhea, failure to thrive, stunted growth, or an increase in gas production.  Often the animals have an increased appetite manifested as polyphagia, coprophagia, or pica.  

• Secondary SIBO:  This is a sequela to a number of primary conditions including chronic Giardia, EPI, motility disorders, intestinal obstruction, or dietary sensitivity.  Clinical signs usually pertain to the primary condition.

Gross Pathology:  There are no gross lesions associated with SIBO.

Histopathology:  Increased bacteria are not evident on tissue biopsy, and there are generally no morphologic changes in SIBO.  Occasionally, histopathology may reveal villous atrophy or mild lymphocytic-plasmocytic inflammation.  In such cases, it is sometimes difficult to determine which came first - the inflammation or the bacterial overgrowth.

• Idiopathic SIBO:  Young, large-breed dogs and German Shepards seem to be more likely to have idiopathic SIBO.  Idiopathic SIBO is not recognized in cats.  

• Secondary SIBO:  This condition may be seen in all breeds and ages of dogs.

Diagnosis:

• The diagnostic gold standard is finding an increased bacterial colony count in duodenal fluid culture via endoscopy.  Colony counts >10⁵ are considered indicative of SIBO. However, some dogs and cats have colony counts as high as 10⁷ -10⁸ and are asymptomatic.  In reality, the test is technically complicated, time-consuming and expensive.  Few veterinarians have the capability of performing the test and in light of the problems associated with interpretation, quantitative culture of duodenal fluid is seldom done.  Instead, veterinarians rely on indirect testing - namely measuring serum folate and cobalamin levels (see below & your clinical pathology notes).

• Increased serum folate, secondary to bacterial synthesis, is commonly associated with SIBO.

• Decreased serum cobalamin is also associated with SIBO because bacterial bind the vitamin cobalamin.
  
  
• The colonic flora does not necessarily reflect what is happening in the small intestine and, therefore, colonic or fecal cultures cannot be used to diagnose SIBO.  

NOTE: An increased serum folate and decreased serum cobalamin is found in both SIBO and Exocrine Pancreatic Insufficiency.  If EPI has been ruled out by a normal TLI, elevated folate in conjunction with decreased serum cobalamin is highly specific for SIBO.  However, it should be noted that these tests are not considered to be very sensitive measures for SIBO.  For more information, see folate and cobalamin.

For more information. . .

• Textbook of Veterinary Internal Medicine: Disease of the dog and cat, 5th edition, eds. Ettinger and Feldman, pp 1223-1228.
• Small Animal Medicine, eds. Nelson and Couto, pp 453.
• Strombeck's Small Animal Gastroenterology, third edition, eds. Guilford, Center, Strombeck, Williams, and Meyer, pp 370-373.