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Small Bowel Bacterial Overgrowth

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<strong>Small</strong> <strong>Bowel</strong> <strong>Bacterial</strong> <strong>Overgrowth</strong><br />

Stephen A. McClave,MD<br />

Professor of Medicine<br />

University of Louisville School of Medicine<br />

Louisville, Kentucky


Introduction<br />

• Definition<br />

Abnormal bacterial proliferation in upper SB<br />

>10,000 colony forming units (cfu/ml)<br />

Syndrome of weight loss, diarrhea and malnutrition<br />

Malabsorption of macro and micronutrients<br />

• History<br />

1897 - Association between bowel strictures and Vit<br />

B 12 deficiency (pernicious anemia)<br />

1939 - Association due to bowel stasis and bacterial<br />

overgrowth (“putrefaction”)


Normal Intestinal<br />

Ecology<br />

• <strong>Bowel</strong> colonization<br />

Sterile (birth) → Full flora at 1 month<br />

Factors – Gestational age,<br />

delivery, feeds<br />

• Levels of colonization<br />

Stomach to jejunum – sterile up to<br />

1,000-10,000<br />

10,000 cfu/ml<br />

Ileum – higher concentration<br />

100,000-1,000,000,000 1,000,000,000 (10 9 ) cfu/ml<br />

Ileocecal valve – steep gradient, some stasis<br />

Colon – Mainly anaerobes<br />

10 9 -10<br />

12 cfu/ml


Variance in <strong>Bacterial</strong> Species<br />

“Good Guys”<br />

“Bad Guys”<br />

Faculative Anaerobes<br />

Gram Positives<br />

True Anaerobes<br />

Gram Negative<br />

Coliforms


Normal Intestinal Ecology<br />

Beneficial Effects of Enteric Bacteria<br />

• <strong>Bacterial</strong> enzymes (disaccharidases) break down carb<br />

sugars to short chain fatty acids to be absorbed in colon<br />

• Some meds require bacterial metabolism for their action<br />

• Enteric bacteria produce folate, vit K<br />

• Enteric nonpathogenic bacteria (“good(<br />

guys”)<br />

prevent colonization by pathogenic orgs (“bad(<br />

guys”)


Host Defense Mechanisms<br />

• Gastric acid<br />

• Intestinal motility<br />

• Intestinal secretions with immunologic properties (IgA)<br />

• Bacteriostatic pancreatic and biliary secretions


Conditions Favoring<br />

SBBO<br />

• Anatomic<br />

SB diverticulosis<br />

Intestinal strictures (Crohn’s, XRT, Ca)<br />

Surgical blind loops (BII, JI bypass)<br />

• Motility disorders<br />

Scleroderma<br />

Diabetic autonomic neuropathy<br />

Idiopathic intestinal pseudoobstruction<br />

• Achlorhydria<br />

Surgical<br />

Atrophic gastritis, chronic H. Pylori


Conditions Favoring SBBO<br />

• Abnormal connections between proximal and distal bowel<br />

Resection IC valve<br />

Fistulas (Crohn’s, PUD, Ca)<br />

• Immunodeficiency states<br />

Common variable immunodefic<br />

Acquired immunodeficiency<br />

Malnutrition<br />

• Other conditions<br />

Cirrhosis<br />

End-stage renal disease<br />

Chronic pancreatitis<br />

Fistula


Pathogenesis of SBBO<br />

• Fat malabsorption<br />

Bacteria unravel (deconjugate) ) bile acids<br />

A toxic lithocholic acid is produced<br />

Action of bile salts


Gut<br />

Lumen<br />

Brush<br />

Border<br />

Pathogenesis<br />

of SBBO<br />

Carbohydrate metabolism<br />

Bacteria digest carbs<br />

Fermentation (hydrogen, CO 2 )<br />

Maldigestion, , osmotic load,<br />

diarrhea, pain


Pathogenesis of SBBO<br />

• Protein metabolism – lesser effect<br />

Bacteria degrade proteins, reduce AA absorption<br />

Less output of pancreatic protease enzymes


Pathogenesis of SBBO<br />

• Alterations in vitamin metabolism<br />

Bacteria utilize Vit B 12<br />

Fat-soluble<br />

Vits A,D,K,E malabsorbed<br />

Bacteria produce folate, Vit K


Clinical features<br />

• Predisposing past history<br />

Surgery<br />

Diabetes<br />

Scleroderma<br />

Crohn’s Disease<br />

Immunodeficiency<br />

Radiation Rx<br />

• Usual symptoms<br />

Asymptomatic<br />

Diarrhea<br />

Weight loss<br />

Abd pain<br />

Bloating<br />

Steatorrhea<br />

• Symptoms related to deficiencies<br />

Night blindness (Vit A)<br />

Osteomalacia (D)<br />

Anemia (B 12 ) Loss of balance (B 12 )


Diagnosis<br />

• <strong>Small</strong> bowel aspirate ( Dx >10 5 cfu/ml )<br />

Special tube to avoid contamination<br />

Best test for now<br />

• Bile acid breath test ( radiolabeled carbon C 14* )<br />

<strong>Bacterial</strong> deconjugation liberates glycine*<br />

Poor test (↓(<br />

specificity, sensitivity)<br />

• D-Xylose<br />

breath test ( radiolabeled carbon C 14 * )<br />

SB absorption occurs before sugar reaches colon<br />

Metabolism produces 14 CO 2 *<br />

Good test (85% pos 1 hr, 100% pos 3 hr)<br />

• Hydrogen breath test<br />

Bacteria ferment carb (lactulose) ) to produce H 2<br />

Early peak (represents SB) vs late peak (represents colon)<br />

Poor test (sensitivity 55%, false pos and neg)


Treatment<br />

• Correct fluid, electrolyte, nutrient deficiencies<br />

• Correct underlying anatomic abnormalities<br />

Surgery<br />

Promotility agents – Reglan, Octreotide,<br />

Erythromycin<br />

• Empiric antibiotic therapy<br />

Rationale – Rx aerobes, O2 kills anaerobes<br />

Examples – TCN, ampicillin, Flagyl, Septra<br />

Monotherapy 7-107<br />

days – Some sustained remission<br />

Rotating combination more effective<br />

• Probiotic therapy – unproven as yet<br />

Examples – Yogurt, lactobacillus GG, Saccharomyces Boulaardi<br />

Promote growth of nonpathogenic “good guys”


Syndrome of<br />

D-Lactic Acidosis<br />

• Definition – Syndrome of<br />

neurologic dysfunction<br />

• Predisposing factors<br />

Short bowel<br />

Intact colon<br />

• Physiology<br />

Fermentation of carbohydrates<br />

Production of D-LactateD<br />

• Diagnosis<br />

Metabolic acidosis<br />

Lab assay for D-Lactate D<br />

(Mayo Clinic)<br />

• Treatment<br />

Limit carbohydrates (simple >> complex)<br />

Antibiotics<br />

TPN, bicarbonate


Conclusions<br />

• Clinical consideration in complex patient<br />

• Identifying likely candidates<br />

• Empiric diagnosis and treatment

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