Gut microbiota is the largest organ of the human body. Although growth of bacteria more than 10 5 colony forming unit (CFU) per milliliter in culture of upper gut aspirate is used to diagnosis small intestinal bacterial overgrowth (SIBO), 10 3 CFU or more is being considered to suggest the diagnosis, particularly if colonic type bacteria are present in the upper gut. Although neither very sensitive nor specific, hydrogen breath tests are widely used to diagnose SIBO. Rifaximin is the best treatment for SIBO due to its broad spectrum, lack of systemic absorption, and safety profile.
Key points
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The role of small intestinal bacterial overgrowth (SIBO) in various intestinal disorders, such as irritable bowel syndrome, celiac and Crohn disease, tropical sprue, gastrointestinal hypomotility states, hypochlorhydria, immunodeficiency states, and structural abnormalities, is increasingly understood.
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Though a bacterial count equal to or greater than 10 5 colony forming unit (CFU)/mL is considered diagnostic of SIBO, some experts suggest that a colony count equal to or greater than 10 3 CFU/mL should also be considered SIBO, particularly if coliforms are present in the upper gut.
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Hydrogen breath tests are popular noninvasive tests using different substrates such as glucose (though highly specific but quite insensitive) and lactulose (early-peak criteria is quite nonspecific and double-peak criteria is quite insensitive) to diagnose SIBO.
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The search for better diagnostic test for SIBO continues.
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Rifaximin is a quite safe and effective agent for treatment and retreatment of SIBO.
Introduction
The gastrointestinal (GI) tract harbors an enormous number of microbes, including bacteria, virus, fungus, and archaea. Interestingly, the microbial cells in the gut (10 14 cells) outnumber that in the human body (10 13 ). Upper gut (stomach, duodenum, and jejunum) is relatively less populated with microbes (0–10 3 bacteria per mL of aspirate) due to the gastric acid barrier ( Fig. 1 ). The microbes in the upper gut are dominated by those that can resist gastric acid, such as Helicobacter pylori and lactobacilli. The distal small bowel and colon have more microbes (10 7 to 10 12 ). Coliforms (Gram-negative nonspore-forming bacilli that ferment lactose) are present exclusively in the distal gut. Gut microbiota performs a variety of functions, such as barrier effect preventing invasion by the pathogenic organisms; regulation of immune function and motility; digestion of food; production of short-chain fatty acids, which regulate colonic water and electrolytes transport and are nutrient to the colonocytes; production of vitamins; metabolism of the drugs; detoxification of toxic compounds; and maintenance of overall homeostasis in the GI tract. Hence, maintenance of normal gut flora (eubiosis) is essential for keeping an individual healthy. Abnormality in the gut flora (dysbiosis), including quantitative increase in small bowel bacteria (ie, small intestinal bacterial overgrowth [SIBO]), qualitative alteration in relative proportion of friendly bacteria and harmful ones, or change in location of bacteria (eg, colonic type bacteria in the small intestine), is known to be associated with several diseases. Definition, etiologic factors, symptomatology, pathophysiology, diagnosis, and treatment of SIBO in relation to various intestinal disorders associated with it are reviewed in this article.
SIBO is defined as overgrowth of bacteria equal to or greater than 10 5 colony forming unit (CFU) per mL of jejunal aspirate. Some authorities suggested that a colony count of equal to or greater than 10 3 CFU/mL of jejunal aspirate should also be considered SIBO, particularly if coliforms are found, especially in irritable bowel syndrome (IBS). Understanding of the importance of SIBO in GI and hepatobiliary diseases is being increasingly recognized over time, as evidenced by publications on this issue ( Fig. 2 ). Table 1 lists the GI and hepatobiliary diseases associated with SIBO.
| Disease | |
|---|---|
| GI diseases | IBS |
| Tropical sprue | |
| Celiac disease | |
| Immunoproliferative small intestinal disease | |
| Inflammatory bowel disease, particularly Crohn disease | |
| Chronic intestinal pseudoobstruction | |
| Collagen diseases with small bowel involvement, such as progressive systemic sclerosis | |
| Gastric and enteric surgery | |
| Short bowel syndrome | |
| Visceral neuropathy (eg, diabetes mellitus, amyloidosis) | |
| Structural causes such as small intestinal diverticula, stricture, and fistula | |
| Lactose malabsorption | |
| Chronic proton pump inhibitor intake | |
| Immune deficiency states (combined variable immunodeficiency, hypogammaglobulinemia, T-cell deficiency) | |
| Hepatic diseases | Cirrhosis of liver |
| Spontaneous bacterial peritonitis | |
| Nonalcoholic fatty liver disease | |
| Pancreatic disease | Chronic pancreatitis due to different causes |
Introduction
The gastrointestinal (GI) tract harbors an enormous number of microbes, including bacteria, virus, fungus, and archaea. Interestingly, the microbial cells in the gut (10 14 cells) outnumber that in the human body (10 13 ). Upper gut (stomach, duodenum, and jejunum) is relatively less populated with microbes (0–10 3 bacteria per mL of aspirate) due to the gastric acid barrier ( Fig. 1 ). The microbes in the upper gut are dominated by those that can resist gastric acid, such as Helicobacter pylori and lactobacilli. The distal small bowel and colon have more microbes (10 7 to 10 12 ). Coliforms (Gram-negative nonspore-forming bacilli that ferment lactose) are present exclusively in the distal gut. Gut microbiota performs a variety of functions, such as barrier effect preventing invasion by the pathogenic organisms; regulation of immune function and motility; digestion of food; production of short-chain fatty acids, which regulate colonic water and electrolytes transport and are nutrient to the colonocytes; production of vitamins; metabolism of the drugs; detoxification of toxic compounds; and maintenance of overall homeostasis in the GI tract. Hence, maintenance of normal gut flora (eubiosis) is essential for keeping an individual healthy. Abnormality in the gut flora (dysbiosis), including quantitative increase in small bowel bacteria (ie, small intestinal bacterial overgrowth [SIBO]), qualitative alteration in relative proportion of friendly bacteria and harmful ones, or change in location of bacteria (eg, colonic type bacteria in the small intestine), is known to be associated with several diseases. Definition, etiologic factors, symptomatology, pathophysiology, diagnosis, and treatment of SIBO in relation to various intestinal disorders associated with it are reviewed in this article.
SIBO is defined as overgrowth of bacteria equal to or greater than 10 5 colony forming unit (CFU) per mL of jejunal aspirate. Some authorities suggested that a colony count of equal to or greater than 10 3 CFU/mL of jejunal aspirate should also be considered SIBO, particularly if coliforms are found, especially in irritable bowel syndrome (IBS). Understanding of the importance of SIBO in GI and hepatobiliary diseases is being increasingly recognized over time, as evidenced by publications on this issue ( Fig. 2 ). Table 1 lists the GI and hepatobiliary diseases associated with SIBO.
| Disease | |
|---|---|
| GI diseases | IBS |
| Tropical sprue | |
| Celiac disease | |
| Immunoproliferative small intestinal disease | |
| Inflammatory bowel disease, particularly Crohn disease | |
| Chronic intestinal pseudoobstruction | |
| Collagen diseases with small bowel involvement, such as progressive systemic sclerosis | |
| Gastric and enteric surgery | |
| Short bowel syndrome | |
| Visceral neuropathy (eg, diabetes mellitus, amyloidosis) | |
| Structural causes such as small intestinal diverticula, stricture, and fistula | |
| Lactose malabsorption | |
| Chronic proton pump inhibitor intake | |
| Immune deficiency states (combined variable immunodeficiency, hypogammaglobulinemia, T-cell deficiency) | |
| Hepatic diseases | Cirrhosis of liver |
| Spontaneous bacterial peritonitis | |
| Nonalcoholic fatty liver disease | |
| Pancreatic disease | Chronic pancreatitis due to different causes |
Etiologic factors and pathogenesis
Fig. 3 enumerates the various factors that predispose to SIBO, which shows that in addition to the structural causes, abnormalities in GI motility and gut defense are risk factors for this condition. Structural causes include intestinal stricture, enteroenteric fistula and anastomosis, diverticula, blind loop syndrome, incompetent ileocecal valve, and various GI surgical procedures, including those reducing gastric acid secretion. Previously, recognition that SIBO can occur in absence of structural causes was somewhat less. However, it is being recognized more and more that a large proportion of patients diagnosed as having SIBO do not have any structural cause.
Normal aboral motility of the gut pushes the intestinal content downward, preventing overgrowth of bacteria in upper gut. In patients with abnormally slow motility, stagnation of intraluminal contents is associated with development of SIBO. Mechanical factors due to previous GI surgery is an important cause of stasis. However, functional stasis is being recognized increasingly as a cause for SIBO. Phase III of fasting intestinal motility, called migratory motor complex (MMC), is an important mechanism to prevent SIBO and abnormal MMC has been shown to be associated with SIBO. Treatment with some prokinetics, such as tegaserod, prevents recurrence of SIBO following its successful treatment. Another mechanism of SIBO in patients with malabsorption syndromes, such as tropical sprue and celiac disease, is slowing of proximal gut motility by its inhibition caused by passage of unabsorbed fat through the ileum-liberating peptide YY, neurotensin, and glucagon-like peptide, a phenomenon called ileal brake ( Fig. 4 ). Hence, a vicious cycle sets in that is associated with slowing of small intestinal motility that leads to further small intestinal bacterial colonization (see Fig. 4 ). Several systemic conditions may be associated with slowing of small intestinal motility, including hypothyroidism; diabetic autonomic neuropathy; other myoneuropathies affecting gut; and collagen diseases, such as progressive systemic sclerosis, systemic lupus erythematosus, and parkinsonism.
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