eMedicine Specialties > Infectious Diseases > Gastrointestinal Tract and Intra-abdominal Infections

Bacterial Overgrowth Syndrome

Author: Pedro A Manibusan Jr, DO, Intern, Department of Internal Medicine, Tripler Army Medical Center
Coauthor(s): Joshua S Hawley, MD, Assistant Chief, Consulting Staff, Departments of Infectious Disease and Internal Medicine, Tripler Army Medical Center; Richard E Frye, MD, PhD, Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Health Science Center at Houston; M Akram Tamer, MD, Program Director, Professor, Department of Pediatrics, University of Miami; Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Contributor Information and Disclosures

Updated: May 21, 2009

Introduction

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, it is now widely accepted that low concentrations of various bacteria 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.

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 gastrointestinal system. Prompt recognition and treatment of bacterial overgrowth syndrome should be targeted to prevent and reverse malabsorptive processes.

Pathophysiology

Normally, colony counts of gram-positive bacteria and fungi in the duodenum and jejunum are less than 1X105 organisms/mL. Aerobic and anaerobic bacterial colony counts in the ileum are usually less than 1X108 organisms/mL. This is in sharp contrast to the 1X1011 organisms/mL that colonize the colon. Studies of duodenal aspirates have not identified any particular bacteria as a cause of bacterial overgrowth syndrome. However, 1X1011 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.

The 5 protective factors listed below 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 reduces the bacteria populations in the proximal small intestine, particularly anaerobic bacteria.
  • The bowel mucosa 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 florae (eg, Lactobacillus) protect 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.

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.

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.21 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 as the cause of wasting in elderly individuals is unknown but is suspected to be significant.

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

Clinical

History

No specific symptoms are pathognomonic for bacterial overgrowth syndrome (BOS). Nonetheless, various nonspecific GI symptoms are common in affected individuals. Clinicians should have a heightened clinical suspicion for bacterial overgrowth syndrome in patients who present with the following:

  • Bloating
  • Flatulence
  • Abdominal pain
  • Diarrhea
  • Dyspepsia
  • Weight loss

Advanced cases of bacterial overgrowth syndrome may manifest as malabsorption findings, as follows:

Physical

A complete physical examination should be performed with emphasis on abdominal examination and examination for signs of malabsorption of various nutrients. No specific physical examination techniques are required for bacterial overgrowth syndrome.

Causes

Disorders or structural abnormalities that disrupt the protective mechanisms that guard against increasing bacterial burden can lead to bacterial overgrowth syndrome.

  • Patients with the following medical conditions are at increased risk for bacterial overgrowth syndrome:
    • History of upper intestinal tract surgery
    • Gastrojejunal anastomosis
    • Vagotomy, but not selective parietal cell vagotomy
    • Antral resection
    • Pancreatic exocrine insufficiency
  • Decreased peristalsis due to the following may result in bacterial overgrowth syndrome:
  • Blind pouches from the following may result in bacterial overgrowth syndrome:
    • Side-to-side or end-to-side anastomoses
    • Intra-abdominal reservoirs
    • Duodenal or jejunal diverticula
    • Segmental dilatation of the ileum
    • Blind loop syndrome
    • Biliopancreatic diversion
    • Chagasic megacolon
  • Abnormal bowel communication due to the following may cause bacterial overgrowth syndrome:
  • Partial obstructions caused by the following may result in bacterial overgrowth syndrome:
  • Reduced gastric acid secretion from the following may result in bacterial overgrowth syndrome:

More on Bacterial Overgrowth Syndrome

Overview: Bacterial Overgrowth Syndrome
Differential Diagnoses & Workup: Bacterial Overgrowth Syndrome
Treatment & Medication: Bacterial Overgrowth Syndrome
Follow-up: Bacterial Overgrowth Syndrome
References

References

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  8. Hill ID, Mann MD, Househam KC, Bowie MD. Use of oral gentamicin, metronidazole, and cholestyramine in the treatment of severe persistent diarrhea in infants. Pediatrics. Apr 1986;77(4):477-81. [Medline].

  9. Hoverstad T, Bjorneklett A, Fausa O, Midtvedt T. Short-chain fatty acids in the small-bowel bacterial overgrowth syndrome. Scand J Gastroenterol. May 1985;20(4):492-9. [Medline].

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  13. Kocoshis SA, Schletewitz K, Lovelace G, Laine RA. Duodenal bile acids among children: keto derivatives and aerobic small bowel bacterial overgrowth [published erratum appears in J Pediatr Gastroenterol Nutr 1988 Jan-Feb;7(1):155]. J Pediatr Gastroenterol Nutr. Sep-Oct 1987;6(5):686-96. [Medline].

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Further Reading

Keywords

bacterial overgrowth syndrome, BOS, acquired monosaccharide intolerance of infancy, blind-loop syndrome, blind loop syndrome, contaminated small bowel syndrome, small intestinal stasis syndrome, stagnant loop syndrome, fat malabsorption, protein malabsorption, carbohydrate malabsorption, vitamin malabsorption, malabsorption, neonatal chronic diarrhea, neonatal diarrhea

Contributor Information and Disclosures

Author

Pedro A Manibusan Jr, DO, Intern, Department of Internal Medicine, Tripler Army Medical Center
Pedro A Manibusan Jr, DO is a member of the following medical societies: American College of Physicians, American Osteopathic Association, and Association of Military Osteopathic Physicians and Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Joshua S Hawley, MD, Assistant Chief, Consulting Staff, Departments of Infectious Disease and Internal Medicine, Tripler Army Medical Center
Joshua S Hawley, MD is a member of the following medical societies: American College of Physicians, Armed Forces Infectious Diseases Society, Infectious Diseases Society of America, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Richard E Frye, MD, PhD, Assistant Professor, Departments of Pediatrics and Neurology, University of Texas Health Science Center at Houston
Richard E Frye, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, Child Neurology Society, and International Neuropsychological Society
Disclosure: Nothing to disclose.

M Akram Tamer, MD, Program Director, Professor, Department of Pediatrics, University of Miami
M Akram Tamer, MD is a member of the following medical societies: American Medical Association and Florida Medical Association
Disclosure: Nothing to disclose.

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Mark Raymond Wallace, MD, Infectious Disease Fellowship Director, Orlando Regional Healthcare; Clinical Professor of Medicine, Florida State University
Mark Raymond Wallace, MD 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

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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