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    Although many aspects of the pathogenesis of salmonella are poorly understood, particularly the relationship between salmonella toxins and cell damage, some of the general features associated with virulence are known. The virulence of salmonellae relates to their ability to invade host cells, replicate in them and resist both digestion by phagocytes and destruction by the complement components of the plasma. Following’s adherence, probably through fimbriae attachment, to the surface of intestinal mucosal cells, the bacteria induce ruffling of cell membranes. The ruffles facilitate uptake of the bacteria in membrane-bound vesicles, which often coalesce. The organisms replicate in these vesicles and are eventually released from the cells, which sustain only mild or transient damage. The complex invasion process is mediated by the products of a number of chromosomal genes, whereas growth within host cells depends on the presence of virulence plasmids. Long chains of LPS prevent the complement components of the membrane attack complex from interacting with and damaging the bacterial cell membrane. The LPS is also responsible for the endotoxic effect of infection with salmonellae. It may contribute to the local inflammatory response which damages intestinal epithelial cells and results in the development of diarrhea. Bacterial cell wall LPS also mediates the endotoxic shock which may accompany septicaemic salmonellosis.

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