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Molecular Pathogenesis of Shigellosis: A Review

One of the earliest steps critical in the pathogenesis of shigellosis is the invasion of shigellae into the epithelial cells (26). The virulent translucent strain of Shigella Ilexneri penetrated intestinal epithelia, whereas the avirulent opaque variant did not, although both had the same parenteral LD50. This observation clearly excluded the then believed hypothesis that the disease is caused by the endotoxin. Virulent shigellae may invade the colonic epithelia by the pathogen-induced internalization and multiplication in the cytoplasm after the phagosomal membrane lysis. This process will be described in this review as the primary invasion as opposed to the secondary invasion of adjacent cells. Successive spread of the bacteria to adjacent cells accompanying their degeneration result in a severe inflammation, leading to the spread of the bacteria to deeper tissue, to an even more severe inflammation and, ultimately, to ulceration and bloody diarrhea. At least three separate virulence determinants on the chromosome of S. flexneri were identified genetically (1 1 13, 15, 48). In addition, Sansonetti and coworkers have established in the early 1980s that a large 100 to 140 MD plasmid is essential for invasion phenotypes (19, 25, 4548). Recent application of recombinant DNA technology and the development of various in vitro assay systems for the virulence phenotypes and advances in cellular and molecular biology have enabled us to make rapid progress in the molecular elucidation of virulence-associated (vir) genes carried by the large plasmid as well as those on the chromosome. Thus, our knowledge on the role of the vir genes has substantially accumulated over the last few years thereby facilitating our understanding of the pathogenesis of shigellosis at the molecular level.