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DR, direct repeat; APEC, avian pathogenic E. coli; UPEC, uropathogenic E. coli; SEPEC, sepsis-causing E. coli; EPEC, enteropatho-genic E. coli; EHEC, enterohemorrhagic E. coli; ETEC, enterotoxigenic E. coli; REPEC, rabbit enteropathogenic E. coli

DR, direct repeat; APEC, avian pathogenic E. coli; UPEC, uropathogenic E. coli; SEPEC, sepsis-causing E. coli; EPEC, enteropatho-genic E. coli; EHEC, enterohemorrhagic E. coli; ETEC, enterotoxigenic E. coli; REPEC, rabbit enteropathogenic E. coli

The genomic island content of the two S.flexneri strains is similar, but their organization and chromosomal insertion site may differ. Shigella pathogenicity islands which have already been analyzed in detail are shown in Table 5.3. Several islands may be involved in niche-specific processes or virulence: the Pic protease/ mucinase and ShETl enterotoxin on the she pathogenicity island (PAI) [26], or the aerobactin siderophore gene cluster on the SHI-2 PAI inserted at selC [27] or on SHI-3 inserted at pheU in S. boydii [28]. Eight other smaller islands contain the sit genes coding for another siderophore system, possible specific adhesins similar to long polar fimbriae (Lpf) or the Saf protein of S. enterica serovar Typhimurium. The most notable island type carries genes related to the type III secreted effector protein IpaH that may support escape of Shigella from macrophage vacuoles. They are secreted by the plasmid-encoded type three secretion system. Five ipaH copies are localized on the virulence plasmid of strain 2457T and seven more are present on the chromosome. Three of them are nonfunctional. In strain 301 four complete and three incomplete ipaH copies have been found on the chromosome as well as five copies on the virulence plasmid pCP301. In both S.flexneri strains, incomplete ipaH copies result from disruption by IS elements or by frameshift mutations [14, 15].

The comparative genome analysis of S.flexneri and E. coli [14, 15] confirms the previous finding that the two are closely related and may belong to the same genus [2, 29]. Shigella evolved from multiple E. coli strains in correlation with the appearance of man much later than, e.g., E.coli O157:H7 and K-12, which diverged from a common ancestor about 4.5 million years ago [6]. To meet the demand of its unique pathogenic lifestyle, the chromosomally determined pheno-typic properties result from convergent evolution during niche adaptation, mostly due to gene acquisition or loss offunction, some from negative selection pressure.

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