Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates

Irene Merino; Stephen B. Porter; Brian Johnston; Connie Clabots; Paul Thuras; Patricia Ruiz-Garbajosa; Rafael Cantón; James R. Johnson

doi:10.1080/21505594.2020.1747799

Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates

Irene Merino, Stephen B. Porter, Brian Johnston, Connie Clabots, Paul Thuras, Patricia Ruiz-Garbajosa, Rafael Cantón, James R. Johnson

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

Background: Escherichia coli ST131, mainly its H30 clade, is the leading cause of extraintestinal E. coli infections but its correlates of virulence are undefined. Materials and methods: We tested in a murine sepsis model 84 ST131 isolates that differed by country of origin (Spain vs. USA), clonal subset, resistance markers, and virulence genes (VGs). Virulence outcomes, including illness severity score (ISS) and “killer” status (>80% mouse lethality), were compared statistically with clonal subset, individual and combined VGs, molecularly defined extraintestinal and uropathogenic E. coli (ExPEC, UPEC) status, and country of origin. Results: Virulence varied widely by strain. Univariable correlates of median ISS and percent “killer” (outcomes if variable present vs. absent) included pap (ISS, 4.4 vs. 3.8; “killer”, 71% vs. 46%), kpsMII (4.1 vs. 2.3; 59% vs. 25%), K2/K100 (4.4 vs. 3.2; 77% vs. 41%), ExPEC (4.2 vs. 2.2; 62% vs. 17%), Spanish origin (4.3 vs. 3.1; 65% vs. 36%), and H30R1 subset (2.5 vs. 4.1; 35% vs. 59%). With multivariable adjustment, ExPEC status was the only consistently significantly predictive variable. Conclusion: Within ST131 the strongest predictor of experimental virulence was molecularly defined ExPEC status. Clonal subsets seemed to behave differently in the murine sepsis model by country of origin.

Original language	English (US)
Pages (from-to)	327-336
Number of pages	10
Journal	Virulence
Volume	11
Issue number	1
DOIs	https://doi.org/10.1080/21505594.2020.1747799
State	Published - Jan 1 2020

Bibliographical note

Funding Information:
Part of this work was supported by Instituto de Salud Carlos III of Spain [grant PI13/02092]); and Spanish Network for Research in Infectious Diseases (REIPI) [RD12/0015/0004, RD16/0016/0011]; a grant from the Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC) [Ayuda a la formaci?n de la SEIMC 2014 to I.M] and co-financed by the European Development Regional Fund (ERDF), ?A Way to Achieve Europe?. I.M. was supported during part of this work by a research contract from the REIPI [RD12/0015/0004; RD16/0016/0011] and is currently supported by a R?o Hortega grant [CM18/00157] by Instituto de Salud Carlos III of Spain. This material also is based partly upon work supported by Office of Research and Development, Medical Research Service, Department of Veterans Affairs [grant # 1 I01 CX000192 01 to JRJ]

Publisher Copyright:
©, This work was authored as part of the Contributor’s official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.

Keywords

E. coli
ExPEC
mouse sepsis model
virulence

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Merino, I., Porter, S. B., Johnston, B., Clabots, C., Thuras, P., Ruiz-Garbajosa, P., Cantón, R., & Johnson, J. R. (2020). Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates. Virulence, 11(1), 327-336. https://doi.org/10.1080/21505594.2020.1747799

Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates. / Merino, Irene; Porter, Stephen B.; Johnston, Brian et al.
In: Virulence, Vol. 11, No. 1, 01.01.2020, p. 327-336.

Research output: Contribution to journal › Article › peer-review

Merino, I, Porter, SB, Johnston, B, Clabots, C, Thuras, P, Ruiz-Garbajosa, P, Cantón, R & Johnson, JR 2020, 'Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates', Virulence, vol. 11, no. 1, pp. 327-336. https://doi.org/10.1080/21505594.2020.1747799

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title = "Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates",

abstract = "Background: Escherichia coli ST131, mainly its H30 clade, is the leading cause of extraintestinal E. coli infections but its correlates of virulence are undefined. Materials and methods: We tested in a murine sepsis model 84 ST131 isolates that differed by country of origin (Spain vs. USA), clonal subset, resistance markers, and virulence genes (VGs). Virulence outcomes, including illness severity score (ISS) and “killer” status (>80% mouse lethality), were compared statistically with clonal subset, individual and combined VGs, molecularly defined extraintestinal and uropathogenic E. coli (ExPEC, UPEC) status, and country of origin. Results: Virulence varied widely by strain. Univariable correlates of median ISS and percent “killer” (outcomes if variable present vs. absent) included pap (ISS, 4.4 vs. 3.8; “killer”, 71% vs. 46%), kpsMII (4.1 vs. 2.3; 59% vs. 25%), K2/K100 (4.4 vs. 3.2; 77% vs. 41%), ExPEC (4.2 vs. 2.2; 62% vs. 17%), Spanish origin (4.3 vs. 3.1; 65% vs. 36%), and H30R1 subset (2.5 vs. 4.1; 35% vs. 59%). With multivariable adjustment, ExPEC status was the only consistently significantly predictive variable. Conclusion: Within ST131 the strongest predictor of experimental virulence was molecularly defined ExPEC status. Clonal subsets seemed to behave differently in the murine sepsis model by country of origin.",

keywords = "E. coli, ExPEC, mouse sepsis model, virulence",

author = "Irene Merino and Porter, {Stephen B.} and Brian Johnston and Connie Clabots and Paul Thuras and Patricia Ruiz-Garbajosa and Rafael Cant{\'o}n and Johnson, {James R.}",

note = "Funding Information: Part of this work was supported by Instituto de Salud Carlos III of Spain [grant PI13/02092]); and Spanish Network for Research in Infectious Diseases (REIPI) [RD12/0015/0004, RD16/0016/0011]; a grant from the Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC) [Ayuda a la formaci?n de la SEIMC 2014 to I.M] and co-financed by the European Development Regional Fund (ERDF), ?A Way to Achieve Europe?. I.M. was supported during part of this work by a research contract from the REIPI [RD12/0015/0004; RD16/0016/0011] and is currently supported by a R?o Hortega grant [CM18/00157] by Instituto de Salud Carlos III of Spain. This material also is based partly upon work supported by Office of Research and Development, Medical Research Service, Department of Veterans Affairs [grant # 1 I01 CX000192 01 to JRJ] Publisher Copyright: {\textcopyright}, This work was authored as part of the Contributor{\textquoteright}s official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.",

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T1 - Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates

AU - Merino, Irene

AU - Porter, Stephen B.

AU - Johnston, Brian

AU - Clabots, Connie

AU - Thuras, Paul

AU - Ruiz-Garbajosa, Patricia

AU - Cantón, Rafael

AU - Johnson, James R.

N1 - Funding Information: Part of this work was supported by Instituto de Salud Carlos III of Spain [grant PI13/02092]); and Spanish Network for Research in Infectious Diseases (REIPI) [RD12/0015/0004, RD16/0016/0011]; a grant from the Spanish Society of Infectious Diseases and Clinical Microbiology (SEIMC) [Ayuda a la formaci?n de la SEIMC 2014 to I.M] and co-financed by the European Development Regional Fund (ERDF), ?A Way to Achieve Europe?. I.M. was supported during part of this work by a research contract from the REIPI [RD12/0015/0004; RD16/0016/0011] and is currently supported by a R?o Hortega grant [CM18/00157] by Instituto de Salud Carlos III of Spain. This material also is based partly upon work supported by Office of Research and Development, Medical Research Service, Department of Veterans Affairs [grant # 1 I01 CX000192 01 to JRJ] Publisher Copyright: ©, This work was authored as part of the Contributor’s official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.

PY - 2020/1/1

Y1 - 2020/1/1

N2 - Background: Escherichia coli ST131, mainly its H30 clade, is the leading cause of extraintestinal E. coli infections but its correlates of virulence are undefined. Materials and methods: We tested in a murine sepsis model 84 ST131 isolates that differed by country of origin (Spain vs. USA), clonal subset, resistance markers, and virulence genes (VGs). Virulence outcomes, including illness severity score (ISS) and “killer” status (>80% mouse lethality), were compared statistically with clonal subset, individual and combined VGs, molecularly defined extraintestinal and uropathogenic E. coli (ExPEC, UPEC) status, and country of origin. Results: Virulence varied widely by strain. Univariable correlates of median ISS and percent “killer” (outcomes if variable present vs. absent) included pap (ISS, 4.4 vs. 3.8; “killer”, 71% vs. 46%), kpsMII (4.1 vs. 2.3; 59% vs. 25%), K2/K100 (4.4 vs. 3.2; 77% vs. 41%), ExPEC (4.2 vs. 2.2; 62% vs. 17%), Spanish origin (4.3 vs. 3.1; 65% vs. 36%), and H30R1 subset (2.5 vs. 4.1; 35% vs. 59%). With multivariable adjustment, ExPEC status was the only consistently significantly predictive variable. Conclusion: Within ST131 the strongest predictor of experimental virulence was molecularly defined ExPEC status. Clonal subsets seemed to behave differently in the murine sepsis model by country of origin.

AB - Background: Escherichia coli ST131, mainly its H30 clade, is the leading cause of extraintestinal E. coli infections but its correlates of virulence are undefined. Materials and methods: We tested in a murine sepsis model 84 ST131 isolates that differed by country of origin (Spain vs. USA), clonal subset, resistance markers, and virulence genes (VGs). Virulence outcomes, including illness severity score (ISS) and “killer” status (>80% mouse lethality), were compared statistically with clonal subset, individual and combined VGs, molecularly defined extraintestinal and uropathogenic E. coli (ExPEC, UPEC) status, and country of origin. Results: Virulence varied widely by strain. Univariable correlates of median ISS and percent “killer” (outcomes if variable present vs. absent) included pap (ISS, 4.4 vs. 3.8; “killer”, 71% vs. 46%), kpsMII (4.1 vs. 2.3; 59% vs. 25%), K2/K100 (4.4 vs. 3.2; 77% vs. 41%), ExPEC (4.2 vs. 2.2; 62% vs. 17%), Spanish origin (4.3 vs. 3.1; 65% vs. 36%), and H30R1 subset (2.5 vs. 4.1; 35% vs. 59%). With multivariable adjustment, ExPEC status was the only consistently significantly predictive variable. Conclusion: Within ST131 the strongest predictor of experimental virulence was molecularly defined ExPEC status. Clonal subsets seemed to behave differently in the murine sepsis model by country of origin.

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Molecularly defined extraintestinal pathogenic Escherichia coli status predicts virulence in a murine sepsis model better than does virotype, individual virulence genes, or clonal subset among E. coli ST131 isolates

Abstract

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