<i>Yersinia</i>
            High-Pathogenicity Island Contributes to Virulence in
            <i>Escherichia coli</i>
            Causing Extraintestinal Infections

Schubert, Sören; Picard, Bertrand; Gouriou, S.; Heesemann, Jürgen; Denamur, Erick

doi:10.1128/iai.70.9.5335-5337.2002

Cited by 134 publications

(135 citation statements)

References 18 publications

(22 reference statements)

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“…The HPI was first described in Yersinia spp., but has also been described in other Enterobacteriaceae (Bach et al, 2000;Koczura & Kaznowski, 2003;Mokracka et al, 2004;Petermann et al, 2008;Schubert et al, 1998Schubert et al, , 2000Schubert et al, , 2002. Yersinia spp., Escherichia coli, and possibly K. pneumoniae isolates containing the HPI are more virulent than isolates lacking this island (Bearden et al, 1997;Carniel et al, 1992;de Almeida et al, 1993;Lin et al, 2008;Schubert et al, 2002). The HPI was recently shown to be transferable by conjugation with HPI-ICEKp1 (Lin et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Indisputable evidence that HPI increased the virulence of the EHOS is lacking. However, in all Enterobacteriaceae tested, virulence was significantly increased by the HPI (Bearden et al, 1997;Carniel et al, 1992;de Almeida et al, 1993;Lin et al, 2008;Schubert et al, 2002). Other genes associated with the EHOS were those previously described on the pLVPK virulence plasmid of K. pneumoniae CG43 (Chen et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Thirty-two of the 100 DNA fragments were directly linked to transferable elements. Seven DNA fragments (size from 967 to 1511 bp) without any sequence overlap contained sequences present in the high pathogenicity island (HPI), which is a 35-76 kb large genomic island and a known virulence factor in Enterobacteriaceae (Bearden et al, 1997;Carniel et al, 1992;de Almeida et al, 1993;Lin et al, 2008;Schubert et al, 2002). Five of these seven DNA fragments belonged to the 25 DNA fragments most highly associated with the EHOS.…”

Section: Potential Virulence Genes In the Ehos (Outbreak I)mentioning

confidence: 99%

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Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Paauw

Caspers²,

Hall

et al. 2009

Microbiology

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Bacterial strains differ in their ability to cause hospital outbreaks. Using comparative genomic hybridization, Enterobacter cloacae complex isolates were studied to identify genetic markers specific for Enterobacter cloacae complex outbreak strains. No outbreak-specific genes were found that were common in all investigated outbreak strains. Therefore, the aim of our study was to identify specific genetic markers for an Enterobacter hormaechei outbreak strain (EHOS) that caused a nationwide outbreak in The Netherlands. Most EHOS isolates carried a large conjugative plasmid (pQC) containing genes encoding heavy-metal resistance, mobile elements, pili-associated proteins and exported proteins as well as multiple-resistance genes. Furthermore, the chromosomally encoded high-pathogenicity island (HPI) was highly associated with the EHOS strain. In addition, other DNA fragments were identified that were associated with virulence: three DNA fragments known to be located on a virulence plasmid (pLVPK), as well as phage-and plasmid-related sequences. Also, four DNA fragments encoding putative pili with the most homology to pili of Salmonella enterica were associated with the EHOS. Finally, four DNA fragments encoding putative outer-membrane proteins were negatively associated with the EHOS. In conclusion, resistance and putative virulence genes were identified in the EHOS that may have contributed to increased epidemicity. The high number of genes detected in the EHOS that were related to transferable elements reflects the genomic plasticity of the E. cloacae complex and may explain the emergence of the EHOS in the hospital environment. INTRODUCTIONIn the pre-antibiotic era, isolates of the Enterobacter cloacae complex were not detected in surveys of nosocomial bacteria; they were first described as nosocomial pathogens in the 1970s (Sanders & Sanders, 1997). In 2001, Enterobacter spp. caused 7 % of nosocomial infections in intensive care units in the USA (Jones, 2003;Streit et al., 2004). Therefore, the E. cloacae complex can be considered as an emerging pathogen, of which Enterobacter hormaechei is the most commonly isolated nosocomial pathogen (Delmas et al., 2006;Paauw et al., 2008). A nationwide outbreak occurred with an E. hormaechei outbreak strain (EHOS) in The Netherlands . This strain disseminated throughout hospitals despite adequate implementation of internationally accepted infection-prevention guidelines and caused invasive infections in more than 100 patients (Paauw et al., 2007). Previous studies showed that most EHOS isolates carried the conjugative plasmid pQC, with several complex integrons containing aadB, bla CTX-M-9 and qnrA1 genes that encoded resistance to aminoglycosides and thirdgeneration cephalosporins, and reduced susceptibility to fluoroquinolones, respectively . However, it was also shown that other Enterobacteriaceae including other E. cloacae complex isolates with the pQC did not become highly epidemic like the EHOS (Paauw et al., 2007). Furthermore, of aminoglycoside-susceptible E. cloa...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Potential Virulence Genes In the Ehos (Outbreak I)mentioning

confidence: 99%

See 1 more Smart Citation

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Paauw

Caspers²,

Hall

et al. 2009

Microbiology

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“…A substantial number of both groups contained genes involved in the formation of different adhesins, including P (various pap genes and alleles) and type 1 fimbriae. APEC and UPEC isolates also contained many genes related to iron acquisition, including fyuA and irp-2, genes of the yersiniabactin operon (Oelschlaeger et al, 2002a;Pelludat et al, 1998;Schubert et al, 1998Schubert et al, , 2000Schubert et al, , 2002; iucC and iutA, genes of the aerobactin operon ; iroN of the salmochelin operon (Russo et al, 2002;Hantke et al, 2003); and sitA of the sit operon (Runyen-Janecky et al, 2003). They also had a high prevalence of genes related to Fig.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Escherichia coli isolates implicated in human urinary tract infection and avian colibacillosis

et al. 2005

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Since avian pathogenic Escherichia coli (APEC) and human uropathogenic E. coli (UPEC) may encounter similar challenges when establishing infection in extraintestinal locations, they may share a similar content of virulence genes and capacity to cause disease. In the present study, 524 APEC and 200 UPEC isolates were compared by their content of virulence genes, phylogenetic group, and other traits. The two groups showed substantial overlap in terms of their serogroups, phylogenetic groups and virulence genotypes, including their possession of certain genes associated with large transmissible plasmids of APEC. Based on these results, the propensity of both groups to cause extraintestinal infections, and a well-documented ability of avian E. coli to spread to human beings, the potential for APEC to act as human UPEC or as a reservoir of virulence genes for UPEC should be considered. However, significant differences in the prevalence of the traits occurred across the two groups, suggesting that if APEC are involved in human urinary tract infections, they are not involved in all of them.

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“…Apart from plasmid-borne factors, genes encoding for ferric yersiniabactin uptake (fyuA) and iron-repressible protein (irp2) have been detected by PCR in more than 65% of strains isolated from cases of avian colibacillosis (Janssen et al, 2001). Subsequent work has shown that production of yersiniabactin contributes to virulence of exPEC and Klebsiella pneumoniae in mice (Schubert et al, 2002;Lawlor et al, 2007). Additionally, chuA (encoding a haeme utilization/transport protein) was detected by screening a signature-tagged mutagenesis bank of APEC O2 in chickens (Li et al, 2005), suggesting a role in virulence.…”

Section: Progress Towards Unravelling Apec Virulence Factorsmentioning

confidence: 99%

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

Dziva¹,

Stevens²

2008

Avian Pathology

298

222

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Avian colibacillosis is caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC). Despite being known for over a century, avian colibacillosis remains one of the major endemic diseases afflicting the poultry industry worldwide. Autologous bacterins provide limited serotype-specific protection, yet multiple serogroups are associated with disease, especially O1, O2 and O78 among many others. Experimental infection models have facilitated the identification of some key APEC virulence genes and have allowed testing of vaccine candidates. Well-recognized virulence factors include Type 1 (F1) and P (Pap/ Prs) fimbriae for colonization, IbeA for invasion, iron acquisition systems, TraT and Iss for serum survival, K and O antigens for anti-phagocytic activity, and a temperature-sensitive haemagglutinin of imprecise function. Intriguingly, these factors do not occur universally among APEC, suggesting the presence of multiple alternative mechanisms mediating pathogenicity. The recent availability of the first complete APEC genome sequence can be expected to accelerate the identification of bacterial genes expressed during infection and required for virulence. High-throughput molecular approaches like signature-tagged transposon mutagenesis have already proved invaluable in revealing portfolios of genes expressed by pathogenic bacteria during infection, and this has enabled identification of APEC O2 factors required for septicaemia in the chicken model. Complimentary approaches, such as in vivo-induced antigen technology, exist to define the activities of APEC in vivo. In recent years, reverse vaccinology and immuno-proteomic approaches have also enabled identification of novel vaccine candidates in other bacterial pathogens. Collectively, such information provides the basis for the development or improvement of strategies to control APEC infections in the food-producing avian species.

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Yersinia High-Pathogenicity Island Contributes to Virulence in Escherichia coli Causing Extraintestinal Infections

Cited by 134 publications

References 18 publications

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Comparison of Escherichia coli isolates implicated in human urinary tract infection and avian colibacillosis

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

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