A New O-Antigen Gene Cluster Has a Key Role in the Virulence of the
            <i>Escherichia coli</i>
            Meningitis Clone O45:K1:H7

Plainvert, Céline; Bidet, Philippe; Peigne, Chantal; Barbe, Valérie; Médigue, Claudine; Denamur, Erick; Bingen, Édouard; Bonacorsi, Stéphane

doi:10.1128/jb.01013-07

Cited by 43 publications

(41 citation statements)

References 42 publications

(39 reference statements)

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“…It is known that Salmonella enterica and Citrobacter freundii share similar but sequence-diversified O-AGCs with E. coli O157, O111, and O55 but produce O antigens that are identical to those produced by E. coli (18). Plainvert et al (19) showed that there are two types of O-AGCs in E. coli O45 strains; one type is related to intestinal pathogenic E. coli such as STEC, and the other is related to extraintestinal pathogenic E. coli. These two O-AGCs are genetically related but show low or no DNA sequence homology in orthologous genes (19).…”

Section: Discussionmentioning

confidence: 99%

“…Plainvert et al (19) showed that there are two types of O-AGCs in E. coli O45 strains; one type is related to intestinal pathogenic E. coli such as STEC, and the other is related to extraintestinal pathogenic E. coli. These two O-AGCs are genetically related but show low or no DNA sequence homology in orthologous genes (19). Sequence variations among the O-AGCs of some strains within the same O serogroups may explain the lack of PCR products in this study.…”

Section: Discussionmentioning

confidence: 99%

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Escherichia coli O-Genotyping PCR: a Comprehensive and Practical Platform for Molecular O Serogrouping

et al. 2015

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Each set contained six to nine primer pairs that amplify products of markedly different sizes. This genetic methodology (E. coli O-genotyping PCR) allowed for comprehensive, rapid, and low-cost typing. Validation of the PCR system using O-serogroup references and wild strains showed that the correct O serogroups were specifically and accurately identified for 100% (182/182) and 90.8% (522/575) of references and wild strains, respectively. The PCR-based system reported here might be a promising tool for the subtyping of E. coli strains for epidemiological studies as well as for the surveillance of pathogenic E. coli during outbreaks.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Escherichia coli O-Genotyping PCR: a Comprehensive and Practical Platform for Molecular O Serogrouping

et al. 2015

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“…The genome and plasmid of strain S88 were sequenced as part of a whole-genome sequencing project (ColiScope [www.genoscope.cns.fr]) at the Evry Genoscope in France. Sequencing and assembly of pS88 were performed as previously described (7,50). MaGe (Magnifying Genomes) software was used for gene annotation and comparative analysis of the S88 genome as described elsewhere (50,63).…”

Section: Methodsmentioning

confidence: 99%

“…The primers used for insertional mutation are listed in Table 2. Correct introduction of the cat gene into the target was controlled by PCR using primers homologous to the cat gene and the flanking region of the target, as previously described (47,50). For each mutant thus obtained, we checked the expression of the K1 capsule antigen, bacteriocin production, the presence of nondeleted plasmid genes, and chromosomal virulence genes, using multiplex PCRs.…”

Section: Vol 77 2009 Virulence Plasmid In E Coli Meningitis Strainmentioning

confidence: 99%

“…S88 mutants were obtained with the PCR-based method of Datsenko and Wanner (19) as previously described, with plasmids kindly provided by Lionello and Nara Bossi (Centre de Génétique Moléculaire, CNRS, Gif sur Yvette, France) (47,50). The primers used for insertional mutation are listed in Table 2.…”

Section: Vol 77 2009 Virulence Plasmid In E Coli Meningitis Strainmentioning

confidence: 99%

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The Plasmid of Escherichia coli Strain S88 (O45:K1:H7) That Causes Neonatal Meningitis Is Closely Related to Avian Pathogenic E. coli Plasmids and Is Associated with High-Level Bacteremia in a Neonatal Rat Meningitis Model

et al. 2009

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A new Escherichia coli virulent clonal group, O45:K1, belonging to the highly virulent subgroup B2 1 was recently identified in France, where it accounts for one-third of E. coli neonatal meningitis cases. Here we describe the sequence, epidemiology and function of the large plasmid harbored by strain S88, which is representative of the O45:K1 clonal group. Plasmid pS88 is 133,853 bp long and contains 144 protein-coding genes. It harbors three different iron uptake systems (aerobactin, salmochelin, and the sitABCD genes) and other putative virulence genes (iss, etsABC, ompT P , and hlyF). The pS88 sequence is composed of several gene blocks homologous to avian pathogenic E. coli plasmids pAPEC-O2-ColV and pAPEC-O1-ColBM. PCR amplification of 11 open reading frames scattered throughout the plasmid was used to investigate the distribution of pS88 and showed that a pS88-like plasmid is present in other meningitis clonal groups such as O18:K1, O1:K1, and O83:K1. A pS88-like plasmid was also found in avian pathogenic strains and human urosepsis strains belonging to subgroup B2 1 . A variant of S88 cured of its plasmid displayed a marked loss of virulence relative to the wild-type strain in a neonatal rat model, with bacteremia more than 2 log CFU/ml lower. The salmochelin siderophore, a known meningovirulence factor, could not alone explain the plasmid's contribution to virulence, as a salmochelin mutant displayed only a minor fall in bacteremia (0.9 log CFU/ml). Thus, pS88 is a major virulence determinant related to avian pathogenic plasmids that has spread not only through meningitis clonal groups but also human urosepsis and avian pathogenic strains.Escherichia coli is the second cause of neonatal bacterial meningitis in industrialized countries, after group B streptococci. Despite advances in neonatal care, E. coli neonatal meningitis (ECNM) remains a potentially devastating illness, with a mortality rate of 10 to 15% and neurological sequelae in 30 to 50% of cases (8,20,28,29,62). Like most extraintestinal pathogenic E. coli (ExPEC) strains, ECNM strains mainly belong to phylogenetic group B2 and compose a small number of

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Mechanisms of Meningeal Invasion by Septicemic Extracellular Pathogens: The Examples ofNeisseria meningitidis,Streptococcus agalactiaeandEscherichia coli

Join‐Lambert

Carbonnelle

Chrétien

et al. 2010

Bacterial Virulence

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Bacterial meningitis is a leading cause of central nervous system infections. It is an infl ammatory process that results from bacterial entry into the subarachnoidal space s ( SAS ). Bacterial meningitis can be due to the dissemination of contiguous infections such as sinusitis or mastoiditis of the meningeal membranes, but most cases are caused by blood -borne pathogens. Unlike other peripheral organs, the central nervous system ( CNS ) is protected from blood -borne insults by specialized structures that separate the nervous parenchyma and the cerebrospinal fl uid from the blood. These blood -brain barrier s ( BBB ) effectively protect the CNS from most circulating bacteria, restricting the etiology of bacterial meningitis to a few and predominantly extracellular pathogens: Escherichia coli K1 and Streptococcus agalactiae (Group B Streptococcus) in the newborn, Neisseria meningitidis , Haemophilus infl uenzae type b and Streptococcus pneumoniae in children and adults [1 -3] . It has been estimated that 63 and 9% of bacteremia due to N. meningitidis and S. pneumoniae, respectively, are associated with meningitis [4] , demonstrating that the ability of these bacteria to enter the subarachnoidal spaces varies. Paradoxically, these bacteria are commensal in the nasopharynx ( N. meningtidis , S. pneumoniae and H. infl uenzae ) and digestive tract ( E. coli , S. agalactiae ) [5] .The pathophysiology of bacterial meningitis is thus a multi -step process that refl ects the ability of bacterial pathogens to cross the oropharyngeal or digestive mucosal barrier, to survive and to multiply in bloodstream and fi nally, to cross the blood -brain barrier [5 -7] . As stated above, the number of bacteria capable of invading the meninges is limited, suggesting that specifi c virulence factors are required for bacteria to enter the subarachnoidal space. Indeed it has been demonstrated that these extracellular pathogens express various virulence factors which allow them to survive in the extracellular fl uids and eventually to interact directly with the components of the blood -brain barrier. The main virulence factor expressed Bacterial Virulence: Basic Principles, Models and Global Approaches. Edited by Philippe Sansonetti

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A New O-Antigen Gene Cluster Has a Key Role in the Virulence of the Escherichia coli Meningitis Clone O45:K1:H7

Cited by 43 publications

References 42 publications

Escherichia coli O-Genotyping PCR: a Comprehensive and Practical Platform for Molecular O Serogrouping

Escherichia coli O-Genotyping PCR: a Comprehensive and Practical Platform for Molecular O Serogrouping

The Plasmid of Escherichia coli Strain S88 (O45:K1:H7) That Causes Neonatal Meningitis Is Closely Related to Avian Pathogenic E. coli Plasmids and Is Associated with High-Level Bacteremia in a Neonatal Rat Meningitis Model

Mechanisms of Meningeal Invasion by Septicemic Extracellular Pathogens: The Examples ofNeisseria meningitidis,Streptococcus agalactiaeandEscherichia coli

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