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Bacterial Overgrowth Syndrome Workup

  • Author: Saqib Zaheer Syed, MBBS; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 17, 2016
 

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 and nutritional evaluation are indicated.

Stool analysis 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.[11] 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.[12] 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.[13] 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.

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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.

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Procedures

Breath tests are used to measure byproducts of bacterial metabolism to identify malabsorbed substances.[14] 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.[15]

Hydrogen breath test

Hydrogen breath tests are based on the fact that in humans hydrogen is exclusively produced by intestinal bacteria, most notably by anaerobic bacteria in the colon of healthy people and also in the small intestine in the case of bacterial overgrowth syndrome. Preoral glucose or lactulose challenge is given before performing hydrogen breath tests. 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. For diagnosis, use 10 g lactulose. A rise in 20 parts per million above baseline is diagnostic. The specificity and sensitivity of this test are 62.5 and 82% after glucose and 56% and 86% after lactulose administration.[16]

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

False positive results may come from disease or resection of terminal ileum, the site of bile absorption. Carbon 14 carries a risk of radiation, which can be problematic in children and pregnant women.[4]

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 14.3-95% and 40-94%, respectively.[4]

Combination of hydrogen breath test with simultaneous D-xylose breath test results in increase in sensitivity of noninvasive diagnostics of bacterial overgrowth syndrome.[17, 18]

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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.

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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 David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Joseph F John, Jr, MD, FACP, FIDSA, FSHEA is a member of the following medical societies: Charleston County Medical Association, Infectious Diseases Society of America, South Carolina Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Pedro A Manibusan Jr, DO; Joshua S Hawley, MD; Richard E Frye, MD, PhD; M Akram Tamer, MD; and Burke A Cunha, MD, to the development and writing of this article.

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