The large virulence plasmid of Shigella.

Abstract

Invasion of human colonic epithelial cells constitutes one of the earliest steps in the pathogenesis of dysentery caused by Shigella species and enteroinvasive strains of Escherichia coli (EIEC). Following the invasion of target cells by virulent bacteria, their subsequent multiplication, intracellular movement, and intercellular spread result in a focus of Shigella infection that is characterized by severe desquamation and ulceration of the mucosa. The first indication that invasion of colonic epithelial cells was critical in the development of the dysenteric syndrome was presented by Labrec et al. (1964) who showed that a virulent, translucent colony morphology strain of Shigella flexneri 2a (2457T) was able to penetrate colonic epithelia in both rhesus monkeys and opiated guinea pigs, whereas an avirulent opaque variant (24570) did not. However, it was not until the early 1980s and the pioneering work of Sansonetti and colleagues that the essential role of a large (100–140MDa) plasmid, found in all virulent strains of Shigella and EEC, was established for the invasion phenotype (Kopecko et al. 1980; Sansonetti et al. 1981,1982,1983b; Harris et al. 1982). Subsequent rapid progress in the study of virulence-related (vir) genes carried by this large invasion plasmid has been complemented by the development of recombinant DNA technology, in vitro assay systems for the various virulence phenotypes, and advances in cellular and molecular biology. As will be reviewed in this chapter, our knowledge of the role of the large plasmid in determining the virulence properties of Shigella has accumulated substantially over the last few years; however, a full characterization of the vir genes has not yet been realized.KeywordsShigella FlexneriLarge PlasmidvirB GeneInvasion PlasmidipaH GeneThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.