Acute diarrhoea is the main cause of mortality and morbidity. Almost five million deaths are attributed to it each year in Africa, Asia and Latin America, essentially before the age of five.
- Under normal conditions, the gastro-intestinal mucosa resists aggressions due to its protective blanket of mucus, and membrane of gastric epithelium cells.
The mucus produced by the epithelium goblet cells is a continuous physical barrier between the underlying tissue and micro-organisms, the toxins they produce, and the antigens present in the intestinal lumen.
Mucus is also a competitive inhibitor for adherence to the epithelial cells.
Adherence is a vital factor in intestinal colonisation. It is achieved by means of the fimbriae or pili, flagella responsible for mobility, by chemotactic factors and by interactions between the bacteria and mucus.
For many bacteria, the specific nature of the interactions is known. On the surface of E. coli, Helicobacter pylori and Yersinia enterocolitica, for example, there are specific proteins called adhesins which often recognise carbohydrates on target cells.
Inhibition of an organism's adhesion to the epithelial cells may be due to similarities between its natural binding site and the mucin's carbohydrates. The protein core of mucins may also contain hydrophobic zones able to form non-covalent bonds with lipids which would protect certain potential receptors from bacteria.
Degradation of mucus phospholipids by Helicobacter pylori could reduce the gastric mucosa's hydrophobic characteristic and promote bacterial interactions with the mucin.
The destruction of disulphide bridges, and hence the depolymerisation and denaturation of mucin in the small intestine, significantly increases adhesion of Y. enterocolitica and certain strains of E. coli. In vitro, in the intestine, the capacity of E. coli to adhere to the enterocyte depends on the presence of a flagellum allowing the bacterium to move.

CLASSIFICATION OF BACTERIA ACCORDING TO SITE AND MECHANISM OF ACTION

Helicobacter pylori
- H. pylori is a spiralled bacterium, mobile due to the presence of 4 to 6 sheathed, unipolar flagella. It is specific to man and a few higher primates. It has the particularity of expressing adhesins able to recognize the specific glycolipid receptors of gastric mucous cells
. Adhesion to the stomach is mediated by fimbrillated structures and results in local abrasion of the microvilli, reduces the thickness of the mucous layer as well as the visco-elasticity and stringiness of the mucus itself, and also alters its hydrophobicity.
Survival of H. pylori in the stomach is due to the synthesis of a very active enzyme on the bacterial surface, urease, which hydrolyses the urea in the gastric juice and releases ammonia.
This is done at very acid pH.
The effect of releasing ammonia is to neutralise the bacterium's environment, allowing it to propagate.
- In the child, H. pylori colonisation causes vomiting, nausea, epigastric pain and even haematemesis. It represents 10 to 15% of indications for paediatric endoscopy. It is only associated with a gastroduodenal ulcer in 11 to 50% of cases while in adults it is virtually systematic. Moreover, on endoscopy, in 50% of cases, it appears as nodular gastritis of the antrum. This lesion occurs in only 15% of adults. It could result in local lymphoid hyperplasia and correspond to the immature immune system's response to initial antigen stimulation by H. pylori at the early stage of infection or even to an exaggerated immune response to a massive initial inoculation in the child.
Histological examination often reveals chronic inflammation and, more rarely, a polynuclear infiltrate.

Invasive bacteria
- E. coli, Campylobacter jejuni and Y. enterocolitica invade the colon and/or small intestine mucosa. There, they cause inflammation and destruction of the mucosa, and are responsible for febrile dysenteric diarrhoea.

- Enteropathogenic E. coli penetrates the glycocalyx, adheres to the surface of colon and small intestine enterocysts without destroying the mucosa or producing toxins. Salmonella does penetrate the colon and small intestine mucosa and may result in systemic invasion.
The bacteria cause a deterioration of the adherent layer of IgA-mucus and promote imbalance of the saprophytic flora.

Toxinogenic bacteria
- Enterotoxinogenic E. coli, Clostridium difficile and Vibrio cholerae attach to the brush border of enterocytes in the small intestine and produce enterotoxins which stimulate the production of cyclic AMP and elicit massive secretion of water and electrolytes in the small intestine and profuse serous diarrhoea, without invading or deteriorating the mucosa.

Cytotoxinogenic bacteria
- They produce both an enterotoxin and a cytotoxin responsible for necrosis of cells damaged by the enterotoxin, and for an inflammatory reaction. Two examples of these are Clostridium difficile and Aeromonas hydrophilia. The latter is a common source of infectious diarrhoea in Asia.


CONCLUSION

All these bacteria cause reactional hypersecretion of mucus and loss of mucus in the intestinal lumen. The role of protection the mucus normally fulfils could be effectively compensated by pharmacological agents such as diosmectite.

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