Abstract
Shigellosis or bacillary dysentery is caused by organisms belonging to genus Shigella, divided into four species (S. dysenteriae, S. boydii, S.flexneri and S. sonnei). With the exception of S. sonnei which has a single serotype, each species is divided into several serotypes according to the O-polysaccharide antigen of the cell wall (S. dysenteriae has 12 serotypes, S. flexneri has 6 serotypes, and S. boydii has 18 serotypes). Shigella spp. are invasive organisms that penetrate into the enterocytes of the colon epithelium, escape very quickly from the phagocytic vacuole and multiplicate intracellularly. Although non-motile, shigellae can move on an actin skeleton and spread to adjacent cells. The inflammatory process is usually limited to the lamina propria and does not involve the spread of Shigella deeper, into the submucosa. Pathogenesis in Shigella spp. is associated with a constellation of genes encoded on both the chromosome and a large 140 MDa virulence plasmid. These genes can be divided into two groups: regulatory genes and structural genes. The 140 MDa plasmid encodes for all the genes essential for invasion of Shigella into the epithelium of the colon. Regulatory genes are located on the virulence plasmid or on the chromosome.
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Cohen, D. et al. (1996). Clinical Trials of Shigella Vaccines in Israel. In: Cohen, S., Shafferman, A. (eds) Novel Strategies in the Design and Production of Vaccines. Advances in Experimental Medicine and Biology, vol 397. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1382-1_21
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DOI: https://doi.org/10.1007/978-1-4899-1382-1_21
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