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

Bacterial Overgrowth Syndrome: Differential Diagnoses & Workup

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

Differential Diagnoses

Afferent Loop Syndrome
Intestinal Motility Disorders
Amebiasis
Intestinal Pseudo-obstruction: Surgical Perspective
Carcinoid Tumor, Intestinal
Irritable Bowel Syndrome
Celiac Sprue
Isosporiasis
Crohn Disease
Lactose Intolerance
Cryptosporidiosis
Malabsorption
Cyclospora
Microsporidiosis
Cytomegalovirus
Pancreatitis, Chronic
Diverticulosis, Small Intestinal
Sprue, Tropical
Giardiasis
Ulcerative Colitis
Inflammatory Bowel Disease
VIPomas
Intestinal Fistulas
Whipple Disease

Other Problems to Be Considered

AIDS
Intestinal pseudo-obstruction

Workup

Laboratory Studies

Bacterial overgrowth syndrome (BOS) diagnostic testing should include a workup for diarrhea, anemia, and malabsorption. In the past, retrieval of aspirates from the small intestine itself during endoscopy was the diagnostic tool of choice; however, its use was limited due to low specificity.

  • Standard anemia workup
  • Nutritional evaluation
  • Stool analysis: This can help detect abnormal stool components. The pH may be acidic, and reducing substance may be present in the stool.
  • D-lactic acidosis syndrome can result from carbohydrate fermentation.
    • Lactic acid levels may need to be measured and, if elevated, monitored.
    • D-lactic acid levels, measured in the blood or urine, can help differentiate bacterial overgrowth syndrome from other metabolic causes.
  • Short-chain fatty acid levels may be elevated in the duodenal fluid but not the stool.9
    • Abnormal duodenal short-chain fatty acid levels average approximately 1 µmol/mL, with acetic acid, propionic acid, and n -butyric acid representing 61%, 16%, and 8% of the total, respectively.
    • The average short-chain fatty acid level in a healthy patient is 0.27 µmol/mL, with acetic acid representing 84% of the total.
  • Keto-bile acid concentration in duodenal fluid is increased and correlates with the type of bacterial overgrowth.13 The molar percent of keto-bile acids in normal duodenal fluid is very close to 0, while gram-negative aerobic and anaerobic overgrowth is associated with levels of 32 µmol/mL and 11 µmol/mL, respectively.
  • Urine 4-hydroxyphenylacetic acid levels may be elevated.3
    • Enteric bacteria that possess L-amino acid decarboxylase produce 4-hydroxyphenylacetic acid from dietary tyrosine.
    • Increased excretion has been demonstrated in adults with bacterial overgrowth syndrome.
    • Creatinine levels that exceed 120 mg/g are typical in children with small-bowel disease or bacterial overgrowth syndrome, including children with chronic Giardia lamblia gastroenteritis.
    • Children with severe pancreatic dysfunction secondary to cystic fibrosis also have significantly high levels of this metabolite.
    • A 2% false-positive rate and no false-negative results are found when this test is used to screen healthy control subjects and hospitalized children.

Imaging Studies

Evaluation for malabsorptive processes should include small-bowel follow-through, which is used to evaluate structure and mobility. Strictures, malrotation, diverticulosis, fistulae, and pseudo-obstruction can be found with this technique.

Imaging and examination of the lower GI tract should be considered if upper GI evaluation is nondiagnostic.

Procedures

Breath tests are used to measure byproducts of bacterial metabolism to identify malabsorbed substances.19 Several studies suggest that 3 breath tests are of adequate specificity, but these studies are not in full agreement regarding the exact sensitivity. Studies that compare these tests with duodenal bacterial counts suggest that the xylose breath test yields the highest specificity.

  • Hydrogen breath test
    • Bacteria ferment malabsorbed carbohydrates. Fermentation releases hydrogen gas that is absorbed and excreted by the lungs. Under normal conditions, fermenting bacteria reside in the colon. In bacterial overgrowth syndrome, the exhaled hydrogen concentration rises early, corresponding to small intestinal bacteria fermentation of carbohydrates. Under such conditions, a later rise in exhaled hydrogen may also be detected during large bowel fermentation. Antibiotic administration invalidates this test.
    • For diagnosis, use 1-2 g/kg of glucose, not to exceed 25-50 g. A rise in exhaled hydrogen to 20 parts per million is diagnostic.
    • The specificity and sensitivity of this test are 80% and 20%-75%, respectively.
  • Bile acid breath test
    • Give glycocholate tagged with carbon 14 with a light meal, and collect breath samples at 2, 4, and 6 hours. An abnormal rise in radioactive carbon dioxide levels indicates bacterial deconjugation of glycocholate.
    • The specificity and sensitivity of this test are 60%-76% and 33%-70%, respectively.
  • Xylose breath test
    • Gram-negative bacteria metabolize xylose, resulting in the release of radioactive carbon dioxide.
    • Administer 1 g of D-xylose tagged with carbon 14, as a liquid, after an overnight fast.
    • Measure radioactive breath carbon dioxide at 30, 60, 90, and 120 minutes. An abnormally high carbon dioxide concentration is usually detected within 30-60 minutes.
    • The specificity and sensitivity of this test are 89% and 30%-90%, respectively.

Histologic Findings

Descending duodenal biopsies performed in a group of elderly individuals with bacterial overgrowth syndrome demonstrated that mean villus height, mean crypt depth, and total mucosal thickness may be reduced. These indices are not significantly different from controls after 6 months of treatment of bacterial overgrowth syndrome. A significant drop in the number of intraepithelial lymphocytes is also seen over this observation period. Mucosal atrophy can result in an 80% reduction of intestinal surface area in infants. Once the offending agent is removed, repair of the small bowel progresses slowly. After 2 months, the villi surface area is 63% normal but the microvillous surface area is only 38% normal.

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

  1. Banwell JG, Sherr H. Effect of bacterial enterotoxins on the gastrointestinal tract. Gastroenterology. Sep 1973;65(3):467-97. [Medline].

  2. Bouhnik Y, Alain S, Attar A, et al. Bacterial populations contaminating the upper gut in patients with small intestinal bacterial overgrowth syndrome. Am J Gastroenterol. May 1999;94(5):1327-31. [Medline].

  3. Chalmers RA, Valman HB, Liberman MM. Measurement of 4-hydroxyphenylacetic aciduria as a screening test for small-bowel disease. Clin Chem. Oct 1979;25(10):1791-4. [Medline].

  4. Donald IP, Kitchingmam G, Donald F, Kupfer RM. The diagnosis of small bowel bacterial overgrowth in elderly patients. J Am Geriatr Soc. Jul 1992;40(7):692-6. [Medline].

  5. Gracey M, Burke V, Oshin A, et al. Bacteria, bile salts, and intestinal monosaccharide malabsorption. Gut. Sep 1971;12(9):683-92. [Medline].

  6. Gregg CR. Enteric bacterial flora and bacterial overgrowth syndrome. Semin Gastrointest Dis. Oct 2002;13(4):200-9. [Medline].

  7. Haboubi NY, Lee GS, Montgomery RD. Duodenal mucosal morphometry of elderly patients with small intestinal bacterial overgrowth: response to antibiotic treatment. Age Ageing. Jan 1991;20(1):29-32. [Medline].

  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].

  10. Kilby AM, Dolby JM, Honour P, Walker-Smith JA. Duodenal bacterial flora in early stages of transient monosaccharide intolerance in infants. Arch Dis Child. Mar 1977;52(3):228-34. [Medline].

  11. King CE, Toskes PP. Small intestine bacterial overgrowth. Gastroenterology. May 1979;76(5 Pt 1):1035-55. [Medline].

  12. Klish WJ, Udall JN, Rodriguez JT, et al. Intestinal surface area in infants with acquired monosaccharide intolerance. J Pediatr. Apr 1978;92(4):566-71. [Medline].

  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].

  14. Lin HC. Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome. JAMA. Aug 18 2004;292(7):852-8. [Medline].

  15. Mathias JR, Clench MH. Review: pathophysiology of diarrhea caused by bacterial overgrowth of the small intestine. Am J Med Sci. Jun 1985;289(6):243-8. [Medline].

  16. Meyers JS, Ehrenpreis ED, Craig RM. Small Intestinal Bacterial Overgrowth Syndrome. Curr Treat Options Gastroenterol. Feb 2001;4(1):7-14. [Medline].

  17. Nichols VN, Fraley JK, Evans KD, Nichols BL Jr. Acquired monosaccharide intolerance in infants. J Pediatr Gastroenterol Nutr. Jan 1989;8(1):51-7. [Medline].

  18. Saltzman JR, Russell RM. Nutritional consequences of intestinal bacterial overgrowth. Compr Ther. 1994;20(9):523-30. [Medline].

  19. Sherr HP, Sasaki Y, Newman A, et al. Detection of bacterial deconjugation of bile salts by a convenient breath-analysis technic. N Engl J Med. Sep 16 1971;285(12):656-61. [Medline].

  20. Tamer MA, Santora TR, Sandberg DH. Cholestyramine therapy for intractable diarrhea. Pediatrics. Feb 1974;53(2):217-20. [Medline].

  21. Virally-Monod M, Tielmans D, Kevorkian JP, et al. Chronic diarrhoea and diabetes mellitus: prevalence of small intestinal bacterial overgrowth. Diabetes Metab. Dec 1998;24(6):530-6. [Medline].

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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