A spontaneous 99-kb chromosomal deletion results in multi-antibiotic susceptibility and an attenuation of contact haemolysis in Shigella flexneri 2a

Rajakumar, Kumar; Sasakawa, Chihiro; Adler, Ben

doi:10.1099/00222615-45-1-64

Cited by 22 publications

(24 citation statements)

References 64 publications

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“…It is speculated that the site-specific excisions (e.g. uropathogenic f. coli) or sequential deletions ( Y. pestis, Y. enterocolitica, H. pylori) of pathogenicity islands or other genetic segments from chromosomes of bacterial pathogens may also play a role in the bacterial adaptation to different environments (Rajahumar et a/., 1996).…”

Section: Deletions As Processes Of Adaptation and Genome Plasticitymentioning

confidence: 99%

Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution

Hacker¹,

Blum-Oehler²,

Mühldorfer³

et al. 1997

Molecular Microbiology

1,012

738

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Summary Virulence genes of pathogenic bacteria, which code for toxins, adhesins, invasins or other virulence factors, may be located on transmissible genetic elements such as transposons, plasmids or bacteriophages. In addition, such genes may be part of particular regions on the bacterial chromosome, termed‘pathogenicity islands’(Pais). Pathogenicity islands are found in Gram‐negative as well as in Gram‐positive bacteria. They are present in the genome of pathogenic strains of a given species but absent or only rarely present in those of non‐pathogenic variants of the same or related species. They comprise large DNA regions (up to 200 kb of DNA) and often carry more than one virulence gene, the G+C contents of which often differ from those of the remaining bacterial genome. In most cases, Pais are flanked by specific DNA sequences, such as direct repeats or insertion sequence (IS) elements. In addition, Pais of certain bacteria (e.g. uropathogenic Escherichia coli, Yersinia spp., Helicobacter pylori) have the tendency to delete with high frequencies or may undergo duplications and amplifications. Pais are often associated with tRNA loci, which may represent target sites for the chromosomal integration of these elements. Bacteriophage attachment sites and cryptic genes on Pais, which are homologous to phage integrase genes, plasmid origins of replication or IS elements, indicate that these particular genetic elements were previously able to spread among bacterial populations by horizontal gene transfer, a process known to contribute to microbial evolution.

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Section: Deletions As Processes Of Adaptation and Genome Plasticitymentioning

confidence: 99%

Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution

Hacker¹,

Blum-Oehler²,

Mühldorfer³

et al. 1997

Molecular Microbiology

1,012

738

View full text Add to dashboard Cite

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“…In many cases, resistance genes are found to reside on easily transferable R plasmids. However, chromosomally borne resistance genes have recently been identified in a number of studies (10,15,29,41,42), although the basis of chromosomal resistance has not been widely investigated.…”

mentioning

confidence: 99%

“…Rajakumar et al (42) have described a spontaneous 99-kb chromosomal deletion that results in multi-antibiotic susceptibility in Shigella flexneri 2a YSH6000. The resistance locus carried on the 99-kb element was found to encode resistance determinants to streptomycin, ampicillin, chloramphenicol, and tetracycline.…”

mentioning

confidence: 99%

“…The SRL exhibits similarity in sequence and organization to the antibiotic resistance loci of NR-1, an R plasmid commonly found in Shigella, and transposon Tn2603 (41). Although the nature and exact location of the 99-kb multiple-antibiotic resistance deletable element (MRDE) harboring the SRL have not been determined, it has been mapped to a region of the chromosome on NotI fragment D bounded by the S. flexneri homologs of the Escherichia coli genes ompA and pyrC (42). The instability of the MRDE is reminiscent of the behavior of other large chromosomal regions in E. coli and Yersinia pestis, referred to as pathogenicity islands (PAIs) (7), suggesting that the MRDE may also be a PAI-like element.…”

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confidence: 99%

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Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

et al. 2001

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In this study, we determined the boundaries of a 99-kb deletable element of Shigella flexneri 2a strain YSH6000. The element, designated the multiple-antibiotic resistance deletable element (MRDE), had recently been found to contain a 66-kb pathogenicity island (PAI)-like element (designated the SRL PAI) which carries the Shigella resistance locus (SRL), encoding resistance determinants to streptomycin, ampicillin, chloramphenicol, and tetracycline. The YSH6000 MRDE was found to be flanked by two identical IS91 elements present at the S. flexneri homologs of the Escherichia coli genes putA and mdoA on NotI fragment D. Sequence data from two YSH6000-derived MRDE deletants, YSH6000T and S2430, revealed that deletion of the MRDE occurred between the two flanking IS91 elements, resulting in a single IS91 element spanning the two original IS91 loci. Selection for the loss of tetracycline resistance confirmed that the MRDE deletion occurred reproducibly from the same chromosomal site and also showed that the SRL PAI and the SRL itself were capable of independent deletion from the chromosome, thus revealing a unique set of nested deletions. The excision frequency of the SRL PAI was estimated to be 10 ؊5 per cell in the wild type, and mutation of a P4-like integrase gene (int) at the left end of the SRL PAI revealed that int mediates precise deletion of the PAI.

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“…IS-mediated deletions and tandem amplifications of DNA of 10 to 100 kb have been reported for S. dysenteriae and Yersinia pestis (5,15). Futhermore, S. flexneri serotype 2a carry at least four pathogenicity islands (1,13,16,19,20,22). Pathogenicity islands are large (often more than 30 kb), unstable DNA fragments that carry many virulence-associated genes and mobility genes (including insertion sequences, integrases, transposases, and origin of plasmid replication) (6).…”

Section: Pfge Of Other Shigella Isolates In Renai and The Neighboringmentioning

confidence: 99%

Molecular Epidemiology of Shigella in aTaiwan Township during 1996 to2000

et al. 2003

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A previously identified Shigella flexneri serotype 2a strain was responsible for an outbreak of shigellosis in a Taiwan township in August 1996. In order to find the relationship between this outbreak strain and subsequent Shigella infections in the area, 59, 47, 35, and 20 Shigella isolates recovered in 1997, 1998, 1999, and 2000, respectively, were collected and typed by serological and pulsed-field gel electrophoresis (PFGE) techniques. Of these 161 isolates, 139 isolates were S. flexneri serotype 2a, and one-third of them (47 isolates) exhibited the outbreak pattern. The remaining 92 S. flexneri serotype 2a isolates displayed 49 different NotI-PFGE patterns. Forty-five patterns were closely related to the outbreak pattern, with deletions of three specific NotI fragments occurring with high frequency. While the outbreak strain remained the main cause of shigellosis after the outbreak, the continuous emergence of closely related though poorly transmissible strains from the outbreak strain contributed to the observed annual decrease of shigellosis in the area.

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A spontaneous 99-kb chromosomal deletion results in multi-antibiotic susceptibility and an attenuation of contact haemolysis in Shigella flexneri 2a

Cited by 22 publications

References 64 publications

Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution

Pathogenicity islands of virulent bacteria: structure, function and impact on microbial evolution

Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

Molecular Epidemiology of Shigella in aTaiwan Township during 1996 to2000

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