Published online by Cambridge University Press: 21 August 2009
Shigella invasion and the host inflammatory responses
Shigella cause bacillary dysentery (shigellosis), a disease provoking a severe inflammatory diarrhea in humans and primates. In tropical areas of developing countries, shigellosis is endemic and a major killer of children under 5 years of age. Shigellosis occurs following ingestion of a very small number (100–1000) of bacteria, thus permitting easy spread of the disease by person-to-person contact as well as by the drinking of contaminated water.
Shigella, a Gram-negative bacillus, comprises four species – S. dysenteriae, S. flexneri, S. boydii, and S. sonnei (Pupo et al., 2000; Lan and Reeves, 2002). Shigella is now recognized as a member of Escherichia coli; however, the group of bacteria causing shigellosis is idiomatically called Shigella in this chapter. Shigellosis is also caused by enteroinvasive E. coli (EIEC), a pathogenic E. coli. Shigella and EIEC possess a large 210- to 230-kb plasmid on which the major virulence functions are encoded. Because Shigella has neither adhesins for upper GI tract cells nor flagella, after infection by means of the fecal–oral route the bacteria reach the colon and rectum directly, where they translocate through the epithelial barrier by means of the M cells overlaying the solitary lymphoid nodules (Fig. 2.1; also see Wassef et al., 1989; Sansonetti et al., 1991, 1996). Once they have reached the underlying M cells, Shigella infect the resident macrophages and multiply.