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Bacterial Overgrowth Syndrome
Small-bowel bacterial overgrowth can result from alterations in intestinal anatomy or GI motility, or lack of gastric acid secretion. This condition can lead to vitamin deficiencies, fat malabsorption, and undernutrition. Diagnosis is by breath test or quantitative culture of intestinal fluid aspirate. Treatment is with oral antibiotics.
Under normal conditions, the proximal small bowel contains < 10 5 bacteria/mL, mainly gram-positive aerobic bacteria. This low bacterial count is maintained by normal peristalsis, normal gastric acid secretion, mucus, secretory IgA, and an intact ileocecal valve.
Anatomic alterations of the stomach and/or small intestine promote stasis of intestinal contents, leading to bacterial overgrowth. Conditions that cause or require anatomic alterations include small-bowel diverticulosis, surgical blind loops, postgastrectomy states (especially in the afferent loop of a Billroth II), strictures, or partial obstruction. Intestinal motility disorders associated with diabetic neuropathy, systemic sclerosis, amyloidosis, hypothyroidism, and idiopathic intestinal pseudo-obstruction can also impair bacterial clearance. Achlorhydria and idiopathic changes in intestinal motility may cause bacterial overgrowth in elderly people.
The excess bacteria consume nutrients, including carbohydrates and vitamin B 12 , leading to caloric deprivation and vitamin B 12 deficiency. However, because the bacteria produce folate, this deficiency is rare. The bacteria deconjugate bile salts, causing failure of micelle formation and subsequent fat malabsorption. Severe bacterial overgrowth also damages the intestinal mucosa. Fat malabsorption and mucosal damage can cause diarrhea.
Some clinicians advocate response to empiric antibiotic therapy as a diagnostic test. However, because bacterial overgrowth can mimic other malabsorptive disorders (eg, Crohn disease) and adverse effects of the antibiotics can worsen symptoms, establishing a definitive etiology is preferred.
The standard for diagnosis is quantitative culture of intestinal fluid aspirate showing a bacterial count >10 5 /mL. This method, however, requires endoscopy. Breath tests, using substrates like glucose, lactulose, and xylose, are noninvasive and easy to do. The 14 C-xylose breath test (see Malabsorption Syndromes:Diagnosing the cause of malabsorption) seems to perform better than the other breath tests.
If the anatomic alterations are not due to previous surgery, an upper GI series with small-bowel follow-through should be done to identify predisposing anatomic lesions.
Treatment is with 10 to 14 days of oral antibiotics that cover both aerobic and anaerobic enteric bacteria. Empiric regimens include use of one of the following: tetracycline 250 mg qid, amoxicillin/clavulanic acid 250 to 500 mg tid, cephalexin 250 mg qid, trimethoprim/sulfamethoxazole 160/800 mg bid, metronidazole 250 to 500 mg tid or qid, or rifaximin 400 to 550 mg bid. Antibiotic treatment can be cyclic, if symptoms tend to recur, and changed based on culture and sensitivity. Changing antibiotic treatment may be difficult, however, due to coexistence of multiple bacteria.
Because bacteria metabolize primarily carbohydrates in the intestinal lumen rather than fats, a diet high in fat and low in carbohydrates and fiber is beneficial.
Underlying conditions and nutritional deficiencies (eg, vitamin B 12 ) should be corrected.
Anatomic alterations in stomach or intestines lead to GI stasis and thus bacterial overgrowth.
Bacteria deconjugate bile salts, causing fat malabsorption.
Diagnosis is made using the 14 C-xylose breath test or quantitative culture of intestinal aspirate.
Oral antibiotics are used, and a high-fat, low-carbohydrate diet is followed.
Drug NameSelect Trade
trimethoprimNo US brand name
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