Bacterial Overgrowth Syndrome 

  • Author: Saqib Zaheer Syed, MBBS; Chief Editor: Michael Stuart Bronze, MD   more...
 
Updated: Apr 11, 2011
 

Background

Bacterial overgrowth syndrome (BOS) is a term that describes clinical manifestations that occur when the normally low number of bacteria that inhabit the stomach, duodenum, jejunum, and proximal ileum significantly increases or becomes overtaken by other pathogens.

The upper intestinal tract was once thought to be a sterile environment; however, low concentrations of various bacteria are now widely accepted to live within or attached to its luminal surface. These bacteria are thought to be present from the time of birth and through adulthood, living in symbiosis with the human host. This relationship is thought to be vital for normal digestive processes, immunity, and intestinal development. Bacterial species usually present include lactobacilli, enterococci, oral streptococci, and other gram-positive aerobic or facultative anaerobes.

Various etiological processes can disrupt mechanisms that keep the number of these bacteria low. These include structural abnormalities (congenital or surgical) and disorders that cause decreased gastric acidity, reduced peristaltic activity, and mucosal damage or atrophy. The clinical manifestations of bacterial overgrowth syndrome stem from the increased bacterial burden on the normal functions of the upper GI system. Prompt recognition and treatment of bacterial overgrowth syndrome should be targeted to prevent and reverse malabsorptive processes.

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Pathophysiology

Normally, colony counts of gram-positive bacteria and fungi in the duodenum and jejunum are less than 1X105 organisms/mL. Anaerobic bacteria are not found in the jejunum in healthy people. As many as one third of jejunal aspirates may be sterile in healthy people. Aerobic and anaerobic bacterial colony counts in the ileum are usually less than 1 X 108 organisms/mL. This is in sharp contrast to the 1 X 1011 organisms/mL that colonize the colon. Prevalence of bacteria in different parts of GI tract depends on several factors such as peristalsis, pH, redox potential, bacterial adhesion, bacterial cooperation and antagonism, mucin secretion, diet, and nutrient availability.[1]

Studies of duodenal aspirates have not identified any particular bacteria as a cause of bacterial overgrowth syndrome. However, 1 X 1011 organisms/mL of aspirate fluid is diagnostic for bacterial overgrowth syndrome. Cultures grown from patients with bacterial overgrowth syndrome reveal abnormally large numbers of anaerobic bacteria in addition to normal flora.

Several protective factors stabilize the number and type of bacteria that colonize the upper GI tract. Abnormalities in these mechanisms predispose to bacterial overgrowth.

Two coordinated motor phenomena produce the continuous propulsive peristaltic action of the upper GI tract. Both the migrating motor complex and the migrating action potential complex clear the upper intestine of unwanted bacteria and undigested substances. Desynchronization of these complexes results in diarrhea and weight loss in animal models. Anatomical defects can reduce peristaltic efficacy; for example, blind pouches result in a stagnant portion of the intestine.

Gastric acid and bile destroy many micro-organisms before they leave the stomach.

Enzymatic activity of intestinal, pancreatic, and biliary secretions help destroy bacteria in the small intestine.[2]

The bowel mucosal integrity and mucin layer protect the gut from bacteria.

Immunoglobulin secretion and immune cells (eg, macrophages and lymphocytes) protect the gut from bacteria.

Normal intestinal flora (eg, Lactobacillus) protects the gut from bacterial overgrowth by maintaining a low pH; however, normal flora can facilitate an abnormal intraluminal environment. Abnormal communications produce pathways that allow enteric bacteria to pass between the proximal and distal bowel.

Ileocecal valve prevents retrograde translocation of bacteria from colon to the small intestine.[2]

Malabsorption of bile acids, fats, carbohydrates, proteins, and vitamins results in direct damage to the lining of the luminal surface by bacteria or by transformation of nutrients into toxic metabolites, leading to many of the symptoms of diarrhea and weight loss associated with bacterial overgrowth syndrome. This leads to decreased function of the enterocytes within the intestinal lining and subsequent malabsorption. Diarrhea is potentiated by unabsorbed food products stimulating secretory cells within the colon.

Anaerobes such as Bacteroides fragilis actively deconjugate bile acids, thereby preventing proper bile acid function and enterohepatic circulation.

Fatty acid absorption is reduced because deconjugated bile acids cannot form micelles.

Deconjugated bile acids directly inhibit carbohydrate transporters. These unabsorbed sugars ferment into organic acids, thereby reducing the intraluminal pH and producing osmotic diarrhea. The unconjugated bile acids also damage intestinal enterocytes and induce water secretion by the colonic mucosa.

Loss of bile acids in the stool reduces the bile acid pool.

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Epidemiology

Frequency

United States

The exact prevalence of bacterial overgrowth syndrome is likely underestimated because the clinical manifestations overlap with those of many other malabsorptive and diarrheal disorders. Higher clinical suspicion should be given to individuals with underlying disorders that disrupt the known protective elements that prevent bacterial overgrowth syndrome. For example, approximately 20%-43% of chronic diarrhea cases in patients with diabetes, as well as 50% in neonates, may be associated with bacterial overgrowth syndrome.[3] In many cases, gastric and upper intestinal tract surgery results in bacterial overgrowth syndrome; however, preservation of the normal anatomy and antroduodenal vagal innervation appear to be protective.

The prevalence of bacterial overgrowth syndrome varies depending on the population studied and the diagnostic methods used. In healthy people, BOS has been described in 0-12.5% by the glucose breath test, 20-22% by the lactulose breath test, and 0-35% when the14 C D-xylose breath test is used.[4] Bacterial overgrowth syndrome is more prevalent in elderly population because of diminished gastric acid secretion and consumption of a large number of medications that can cause hypomotility. BOS has also been described as a cause of occult malabsorption in elderly patients.[5]

Mortality/Morbidity

Bacterial overgrowth syndrome can lead to worsening symptoms of malabsorption and diarrhea. In certain patient subgroups, bacterial overgrowth syndrome can lead to significant morbidity or death. However, exact mortality rates directly linked to bacterial overgrowth syndrome are not readily available.

Patient populations at an increased risk of mortality due to bacterial overgrowth syndrome include the following:

  • Neonates and young infants who are already malnourished or have congenital GI abnormalities
  • Elderly patients with multiple medical problems and those who have underlying chronic diarrhea without known bacterial overgrowth syndrome
  • Patients who have undergone prior upper intestinal surgery that alters the protective mechanisms that prevent bacterial overgrowth syndrome
  • Patients with poor nutritional status at presentation
  • Patients with underlying medical conditions such as diabetes and scleroderma, who are at risk for relapse if the underlying medical condition is not corrected or managed
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Contributor Information and Disclosures
Author

Saqib Zaheer Syed, MBBS  Resident Physician, Department of Internal Medicine, University of Oklahoma Health Science Center

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark R Wallace, MD, FACP, FIDSA  Clinical Professor of Medicine, Florida State University College of Medicine; Head of Infectious Disease Fellowship Program, Orlando Regional Medical Center

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Joseph F John Jr, MD, FACP, FIDSA, FSHEA  Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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