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INTESTINE BACTERIAL OVERGROWTH

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The intestinal bacterial flora is regulated by numerous factors: non-specific barriers (gastric pH, intestinal mucus, etc.), immunological barriers, factors related to intestinal anatomy and motricity, intraluminal factors (bile salts, digestive secretions, nutrients, etc.) and bacterial interactions.

Intestinal bacterial overgrowth (IBO) may be defined as the presence of a quantitatively and/or qualitatively abnormal flora in the small intestine causing clinical disorders and/or malabsorption and engendering susceptibility to infectious complications. Such conditions are due to changes in bacterial clearance, compounded by phenomena of micro-organism interference and adhesion.

THE ORIGIN OF BACTERIAL OVERGROWTH


The causes of overgrowth are :

The main consequences of intestine bacterial overgrowth are malabsorption of nutrients and vitamins due to bacterial enzyme activities, deconjugation of bile salts, lesions of the intestinal mucosa, and deteriorated enterocytic enzyme activity.

Mucosal lesions are presented in Table 1.


Mucosal lesions resulting from intralumen bacterial overgrowth

Factors

Mucosal lesions

Volatile acids
Micro-ulceration
Free bile acids
Enzyme deterioration
Bacterial proteases
Permeability changes
Bacterial toxins
Protein-losing enteropathy
Adherent bacteria
Atrophy of the villi

The infectious complications are septicaemia by bacterial translocation, endotoxinaemia and bacterial or toxic hepatitis due to the deconjugation of bile salts.


DIAGNOSIS OF BACTERIAL OVERGROWTH


Diagnosis of IBO is based on clinical and bacteriological analysis.

- On the clinical level, since direct or indirect bacteriological evidence is sometimes hard to provide, diathesis and symptoms (diarrhoea, ballooning, malabsorption, infections) should be considered first.

- On the bacterial level, qualitative and quantitative analysis may be done by examining the duodenal and/or jejunal flora by the corresponding tubage technique, along with analysis of the pharyngeal flora. A concentration (C) > 106/ml is evidence of IBO; the type of germ is determined by gelose cultures in a laboratory experienced in identification and quantification techniques such as these.

The limits to this diagnostic approach are the examination duration, contamination of the sampling probe, the difficulty of demonstrating anaerobes, the quality of bacterial counts and in vitro cultures and, lastly, the sampling site compared to the seat of overgrowth. The result of this is false negatives and false positives. Coprocultures, unless they isolate a abundant monomorphic flora such as a particular strain of pathogenic enterobacteria, are of limited interest.

Indirect methods based on bacterial metabolism include duodenal tubage and assaying of non-conjugated bile acids or volatile fatty acids, urine assays (indicanuria and free phenols/24h) and breath tests using labelled glycocholate (CO2), 14C-xylose (CO2), lactose or lactulose (H2). The methods are limited by the use of stable or radioactive isotopes, the effect of the caecum, and acceleration of transit resulting from a dose of lactulose. Moreover, not all bacteria produce hydrogen.

In practice

Diagnosis is based on analysing the diathesis, proper sampling of duodenal flora, examining the transit time (carmine) both before and during an H2 breath test on an empty stomach and every 15 minutes after a dose of lactulose. Sometimes, the therapeutic test will provide the retrospective "evidence" of IBO.

TREATMENT


Outside antibiotic treatment, surgery is indicated for removing an obstacle or a blind loop or for carrying out an enterostomy. Human milk stimulates motricity and provides bacteriostatic factors.

Antibiotic treatment depends on various strategies which will depend on habits, experience, anatomical or functional indication, as well as the germs involved. It could be monotherapy (erythromycin, tetracyclines, metronidazole), bitherapy (colimycine 500,000 units and metronidazole 10 mg/kg) 3 times/day or (erythromycine 10 mg/kg and metronidazole 10 mg/kg) 3 times/day or even total digestive decontamination (DD); the risk of total DD, however, is the emergence of multiresistant strains.

The criteria of effectiveness for total, partial or selective DD is based on analysis of clinical improvement, measurement of absorption (steatorrhoea and stool weight), the H2 breath test, duodenal flora and/or coprocultures.
Total DD may be performed as emergency treatment for septicaemia of digestive origin (translocation) which is not rapidly brought under full control by systemic antibiotic treatment. This is often the most effective stand, but means a total DD lasting according to aetiology and continuation of the systemic antibiotic treatment.

The use of so-called substitution "floras" or "probiotics" is believed to be effective; they are currently being assessed.

Digestive mucus modifiers could be a useful therapeutic approach because of their capacity to intervene in bacterial adhesion mechanisms. The interactive mechanisms between mucin and bacteria are said to let the latter resist the binding and penetration of micro-organisms and toxins present in the intestinal lumen.

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