Identification and characterization of Escherichia coli RS218-derived islands in the pathogenesis of E. coli meningitis

Yi Xie, Vitaliy Kolisnycheiko, Maneesh Paul-Satyasesla, Simon Elliott, Geetha Parthasarathy, Yirfeng Yao, Guy Plunkett, Frederick R. Blattner, Kwang Sik Kim

Research output: Contribution to journalArticle

Abstract

Background. Escherichia coli K1 is the most common gram-negative bacterium causing neonatal meningitis, but the mechanisms by which E. coli K1 causes meningitis are not clear. Methods. We identified 22 E. coli RS218-derived genomic islands (RDIs), using a comparative genome analysis of meningitis-causing E. coli K1 strain RS218 (O18:K1:H7) and laboratory K-12 strain MG1655. Series of RDI deletion mutants were constructed and examined for phenotypes relevant to E. coli K1 meningitis. Results. We identified 9 RDI deletion mutants (RDI 1, 4, 7, 12, 13, 16, 20, 21, and 22) that exhibited defects in meningitis development. RDI 16 and 21 mutants had profound defects in the induction of a high level of bacteremia in neonatal rats, and RDI 4 mutants exhibited a moderate defect in the induction of bacteremia. RDI 1 and 22 mutants showed defects in the ability to invade human brain microvascular endothelial cells (HBMECs), and RDI 12 mutants were defective in the ability to bind to HBMECs. RDI 13 and 20 mutants were defective in the ability to both bind to and invade HBMECs. RDI 7 mutants were defective in the induction of bacteremia and in the ability to both bind to and invade HBMECs. Conclusions. These results provide a framework for the future discovery and analysis of bacteremia and meningitis caused by E. coli K1 strain RS218.

Original languageEnglish (US)
Pages (from-to)358-364
Number of pages7
JournalJournal of Infectious Diseases
Volume194
Issue number3
DOIs
StatePublished - Aug 1 2006

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Escherichia coli Meningitis
Genomic Islands
Islands
Escherichia coli
Bacteremia
Endothelial Cells
Meningitis
Brain
Gram-Negative Bacteria

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

Identification and characterization of Escherichia coli RS218-derived islands in the pathogenesis of E. coli meningitis. / Xie, Yi; Kolisnycheiko, Vitaliy; Paul-Satyasesla, Maneesh; Elliott, Simon; Parthasarathy, Geetha; Yao, Yirfeng; Plunkett, Guy; Blattner, Frederick R.; Kim, Kwang Sik.

In: Journal of Infectious Diseases, Vol. 194, No. 3, 01.08.2006, p. 358-364.

Research output: Contribution to journalArticle

Xie, Y, Kolisnycheiko, V, Paul-Satyasesla, M, Elliott, S, Parthasarathy, G, Yao, Y, Plunkett, G, Blattner, FR & Kim, KS 2006, 'Identification and characterization of Escherichia coli RS218-derived islands in the pathogenesis of E. coli meningitis', Journal of Infectious Diseases, vol. 194, no. 3, pp. 358-364. https://doi.org/10.1086/505429
Xie, Yi ; Kolisnycheiko, Vitaliy ; Paul-Satyasesla, Maneesh ; Elliott, Simon ; Parthasarathy, Geetha ; Yao, Yirfeng ; Plunkett, Guy ; Blattner, Frederick R. ; Kim, Kwang Sik. / Identification and characterization of Escherichia coli RS218-derived islands in the pathogenesis of E. coli meningitis. In: Journal of Infectious Diseases. 2006 ; Vol. 194, No. 3. pp. 358-364.
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AU - Elliott, Simon

AU - Parthasarathy, Geetha

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N2 - Background. Escherichia coli K1 is the most common gram-negative bacterium causing neonatal meningitis, but the mechanisms by which E. coli K1 causes meningitis are not clear. Methods. We identified 22 E. coli RS218-derived genomic islands (RDIs), using a comparative genome analysis of meningitis-causing E. coli K1 strain RS218 (O18:K1:H7) and laboratory K-12 strain MG1655. Series of RDI deletion mutants were constructed and examined for phenotypes relevant to E. coli K1 meningitis. Results. We identified 9 RDI deletion mutants (RDI 1, 4, 7, 12, 13, 16, 20, 21, and 22) that exhibited defects in meningitis development. RDI 16 and 21 mutants had profound defects in the induction of a high level of bacteremia in neonatal rats, and RDI 4 mutants exhibited a moderate defect in the induction of bacteremia. RDI 1 and 22 mutants showed defects in the ability to invade human brain microvascular endothelial cells (HBMECs), and RDI 12 mutants were defective in the ability to bind to HBMECs. RDI 13 and 20 mutants were defective in the ability to both bind to and invade HBMECs. RDI 7 mutants were defective in the induction of bacteremia and in the ability to both bind to and invade HBMECs. Conclusions. These results provide a framework for the future discovery and analysis of bacteremia and meningitis caused by E. coli K1 strain RS218.

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