Shiga Toxin–producingEscherichia coliStrains Negative for Locus of Enterocyte Effacement

Hayley J Newton,Adrienne W Paton,Dieter M Bulach,James C Paton,Torsten Seemann,Roy M Robins-Browne,Thomas S Whittam,Joan Sloan,Cody C Allison,Elizabeth L Hartland,Marija Tauschek

doi:10.3201/eid1503.080631

Hayley J Newton, Adrienne W Paton + Show 9 more

Open Access

https://doi.org/10.3201/eid1503.080631

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Journal: Emerging Infectious Diseases	Publication Date: Mar 1, 2009
Citations: 129	License type: cc-by

Abstract

Most Shiga toxin-producing Escherichia coli (STEC) infections that are associated with severe sequelae such as hemolytic uremic syndrome (HUS) are caused by attaching and effacing pathogens that carry the locus of enterocyte effacement (LEE). However, a proportion of STEC isolates that do not carry LEE have been associated with HUS. To clarify the emergence of LEE-negative STEC, we compared the genetic composition of the virulence plasmids pO113 and pO157 from LEE-negative and LEE-positive STEC, respectively. The complete nucleotide sequence of pO113 showed that several plasmid genes were shared by STEC O157:H7. In addition, allelic profiling of the ehxA gene demonstrated that pO113 belongs to a different evolutionary lineage than pO157 and that the virulence plasmids of LEE-negative STEC strains were highly related. In contrast, multilocus sequence typing of 17 LEE-negative STEC isolates showed several clonal groups, suggesting that pathogenic LEE-negative STEC has emerged several times throughout its evolution.

Highlights

Most Shiga toxin–producing Escherichia coli (STEC) infections that are associated with severe sequelae such as hemolytic uremic syndrome (HUS) are caused by attaching and effacing pathogens that carry the locus of enterocyte effacement (LEE)
Many studies have demonstrated that LEE is essential for host colonization and virulence of A/E pathogens [6,7,8,9], others have demonstrated that some STEC isolates without LEE, such as STEC O113:H21, are associated with sporadic and outbreak cases of severe disease indistinguishable from that caused by STEC O157:H7 [10,11,12,13]
We performed allelic profiling of ehxA and repA from LEE-negative and LEE-positive STEC isolates to model plasmid evolution compared with the evolution of the E. coli background, which was determined by multilocus sequence typing (MLST)

Summary

Introduction

Most Shiga toxin–producing Escherichia coli (STEC) infections that are associated with severe sequelae such as hemolytic uremic syndrome (HUS) are caused by attaching and effacing pathogens that carry the locus of enterocyte effacement (LEE). Allelic profiling of the ehxA gene demonstrated that pO113 belongs to a different evolutionary lineage than pO157 and that the virulence plasmids of LEEnegative STEC strains were highly related. To clarify the contribution of large plasmids to the virulence and evolution of STEC, we determined the complete nucleotide sequence of pO113 from EH41, a clinical (HUS) isolate of STEC O113:H21 [21]. We performed allelic profiling of ehxA and repA (a plasmid replication initiation gene of pO113) from LEE-negative and LEE-positive STEC isolates to model plasmid evolution compared with the evolution of the E. coli background, which was determined by multilocus sequence typing (MLST). To increase understanding of the evolutionary origins of STEC, we determined genetic features of LEE-negative STEC that may be used to improve diagnosis and detection

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Conclusion