Przeżywalność Bacillus cereus w jelicie cienkim

Bacillus cereus-mediated food poisoning of the diarrhoeal type is related to the production of the following extracellular factors by the bacteria: haemolysin BL (enterotoxin HBL), non-haemolytic toxin (NHE), and cytotoxin (CytK), as well as haemolysins IV and cereolysin O, both of which have been scarcely examined and discussed in the literature. This article reviews the literature containing current data that revise former theories on the pathogenesis of the diarrhoeal form of B. cereus-mediated food poisoning. The results of in vitro studies confirming the survival of vegetative cells in the stomach and intestine environment prove that the biological state of the examined bacteria does not have any influence on the occurrence of the diarrhoeal syndrome. After contaminated food has been ingested, B. cereus spores/vegetative cells pass the stomach and reach the small intestine. There the spores can germinate to become vegetative cells that multiply and produce enterotoxins. The enterotoxins, finally, affect the intestinal epithelium, which results in diarrhoea. So far this type of food poisoning has been attributed to enterotoxin activity, excluding any kind of interaction between the host and the microorganism. However, according to the results of the latest research, the interaction between the epithelial cells and the cells of B. cereus contributes to the occurrence of infection symptoms, and the adhesion of B. cereus to the intestinal epithelium is prerequisite for the onset of the diarrhoeal syndrome. This article illustrates different aspects of B.cereus survival inside the human gastrointestinal tract, paying special attention to its lower part, i. e. the small intestine. The effect of exposure to bile salts and other factors, as well as to the indigenous microflora of the gastrointestinal tract, on B.cereus survival has been discussed. The article also elucidates issues relating to the mechanism of bacterial-epithelial cell cross-talk (interaction), which is induced when a pathogen comes into contact with enterocytes.