(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) > cellular organisms: NE > Bacteria: NE > Proteobacteria: NE > Gammaproteobacteria: NE > Enterobacterales: NE > Enterobacteriaceae: NE > Shigella: NE > Shigella flexneri: NE
Warning: This entry is a compilation of different species or line or strain with more than 90% amino acide identity. You can retrieve all strain data
(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) Shigella dysenteriae 1012: N, E.
Shigella boydii CDC 3083-94: N, E.
Shigella flexneri 2002017: N, E.
Shigella flexneri 5 str. 8401: N, E.
Shigella flexneri CDC 796-83: N, E.
Shigella flexneri 2a str. 2457T: N, E.
Shigella flexneri 5a str. M90T: N, E.
Shigella flexneri J1713: N, E.
Shigella flexneri K-218: N, E.
Shigella flexneri 4343-70: N, E.
Shigella flexneri K-304: N, E.
Shigella flexneri K-671: N, E.
Shigella flexneri VA-6: N, E.
Shigella flexneri K-272: N, E.
Shigella flexneri 2747-71: N, E.
Shigella flexneri K-227: N, E.
Shigella flexneri 2930-71: N, E.
Shigella flexneri 1235-66: N, E.
Shigella flexneri K-1770: N, E.
Shigella flexneri 2850-71: N, E.
Shigella flexneri 1485-80: N, E.
Shigella flexneri 6603-63: N, E.
Shigella flexneri K-404: N, E.
Shigella flexneri CCH060: N, E.
Shigella sonnei Ss046: N, E.
Shigella boydii Sb227: N, E.
Shigella dysenteriae Sd197: N, E.
LegendThis sequence has been compared to family alignement (MSA) red => minority aminoacid blue => majority aminoacid color intensity => conservation rate title => sequence position(MSA position)aminoacid rate Catalytic site Catalytic site in the MSA MICCMLTIVNIAQHFYKGTENTMATTQQSGFAPAASPLASTIVQTPDDAI VAGFTSIPSQGDNMPAYHARPKQSDGPLPVVIVVQEIFGVHEHIRDICRR LALEGYLAIAPELYFREGDPNDFADIPTLLSGLVAKVPDSQVLADLDHVA SWASRNGGDVHRLMITGFCWGGRITWLYAAHNPQLKAAVAWYGKLTGDKS LNSPKQPVDIATDLNAPVLGLYGGQDNSIPQESVETMRQALRAANAKAEI IVYPDAGHAFNADYRPSYHAESAKDGWQRMLEWFKQYGGKKSL
Shigella spp. are the causative agent of shigellosis with Shigella flexneri serotype 2a being the most prevalent in developing countries. Epidemiological surveillance in China found that a new serotype of S. flexneri appeared in 2001 and replaced serotype 2a in 2003 as the most prevalent serotype in Henan Province. The new serotype also became the dominant serotype in 7 of the 10 other provinces under surveillance in China by 2007. The serotype was identified as a variant of serotype X. It differs from serotype X by agglutination to the monovalent anti-IV type antiserum and the group antigen-specific monoclonal antibody MASF IV-I. Genome sequencing of a serotype X variant isolate, 2002017, showed that it acquired a Shigella serotype conversion island, also as an SfX bacteriophage, containing gtr genes for type X-specific glucosylation. Multilocus sequence typing of 15 genes from 37 serotype X variant isolates and 69 isolates of eight other serotypes, 1a, 2a, 2b, 3a, 4a, 5b, X, and Y, found that all belong to a new sequence type (ST), ST91. Pulsed-field gel electrophoresis revealed 154 pulse types with 655 S. flexneri isolates analyzed and identified 57 serotype switching events. The data suggest that S. flexneri epidemics in China have been caused by a single epidemic clone, ST91, with frequent serotype switching to evade infection-induced immunity to serotypes to which the population was exposed previously. The clone has also acquired resistance to multiple antibiotics. These findings underscore the challenges to the current vaccine development and control strategies for shigellosis.
The Shigella bacteria cause bacillary dysentery, which remains a significant threat to public health. The genus status and species classification appear no longer valid, as compelling evidence indicates that Shigella, as well as enteroinvasive Escherichia coli, are derived from multiple origins of E.coli and form a single pathovar. Nevertheless, Shigella dysenteriae serotype 1 causes deadly epidemics but Shigella boydii is restricted to the Indian subcontinent, while Shigella flexneri and Shigella sonnei are prevalent in developing and developed countries respectively. To begin to explain these distinctive epidemiological and pathological features at the genome level, we have carried out comparative genomics on four representative strains. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E.coli K12 strain MG1655, but each has over 200 pseudogenes, 300 approximately 700 copies of insertion sequence (IS) elements, and numerous deletions, insertions, translocations and inversions. There is extensive diversity of putative virulence genes, mostly acquired via bacteriophage-mediated lateral gene transfer. Hence, via convergent evolution involving gain and loss of functions, through bacteriophage-mediated gene acquisition, IS-mediated DNA rearrangements and formation of pseudogenes, the Shigella spp. became highly specific human pathogens with variable epidemiological and pathological features.
We have sequenced the genome of Shigella flexneri serotype 2a, the most prevalent species and serotype that causes bacillary dysentery or shigellosis in man. The whole genome is composed of a 4 607 203 bp chromosome and a 221 618 bp virulence plasmid, designated pCP301. While the plasmid shows minor divergence from that sequenced in serotype 5a, striking characteristics of the chromosome have been revealed. The S.flexneri chromosome has, astonishingly, 314 IS elements, more than 7-fold over those possessed by its close relatives, the non-pathogenic K12 strain and enterohemorrhagic O157:H7 strain of Escherichia coli. There are 13 translocations and inversions compared with the E.coli sequences, all involve a segment larger than 5 kb, and most are associated with deletions or acquired DNA sequences, of which several are likely to be bacteriophage-transmitted pathogenicity islands. Furthermore, S.flexneri, resembling another human-restricted enteric pathogen, Salmonella typhi, also has hundreds of pseudogenes compared with the E.coli strains. All of these could be subjected to investigations towards novel preventative and treatment strategies against shigellosis.
Shigella flexneri, Shigella boydii, Shigella dysenteriae, Shigella sonnei enterochelin esterase