Phylogenetic classification of Escherichia coli O157:H7 strains of human and bovine origin using a novel set of nucleotide polymorphisms

Michael L Clawson,Tara G Mcdaneld,Lisa M Durso,Margaret A Davis,James L Bono,Robert E Mandrell,Timothy Pl Smith,James E Keen

doi:10.1186/gb-2009-10-5-r56

Abstract

Novel SNPs from human and bovine O157:H7 E. coli isolates are mapped, revealing that the majority of human disease is caused by a bovine subset of this strain.

Highlights

Cattle are a reservoir of Shiga toxin-producing Escherichia coli Shiga toxincontaining Escherichia coli O157 (O157):H7 (STEC O157), and are known to harbor subtypes not typically found in clinically ill humans
Heterogeneity between STEC O157 strains has been detected through multilocus sequence tagging [9], octamer and PCRbased genome scanning [10,11], phage typing [12,13], multiple-locus variable-number tandem repeat analysis [14], microarrays [15,16], nucleotide polymorphism assays [8], phage integration patterns coupled with genome polymorphisms [17,18], and pulsed-field gel electrophoresis (PFGE) [19,20]
Phylogenetic trees produced by the genotypes are split into clades that represent strains of cattle origin, or cattle and human origin. These results indicate that heterologous members of the STEC O157 serotype are distinguishable through nucleotide polymorphisms, and support the notion that a subset of STEC O157 harbored in cattle causes the majority of human disease

Summary

Introduction

Cattle are a reservoir of Shiga toxin-producing Escherichia coli O157:H7 (STEC O157), and are known to harbor subtypes not typically found in clinically ill humans. Nucleotide polymorphisms previously discovered via strains originating from human outbreaks may be restricted in their ability to distinguish STEC O157 genetic subtypes present in cattle. The loss and gain of genes through horizontal transfer, coupled with nucleotide variation distributed throughout the STEC O157 genome, serve in both recording the evolution and defining the diversity of this pathogenic serotype [6,7,8]. PFGE is currently the method of choice for distinguishing between STEC O157 strains implicated in outbreaks [21], and entails standardized chromosome digestions with XbaI, and separation of DNA segments through gel electrophoresis[22]. The standardized PFGE method is unreliable for determining genetic relatedness between STEC O157 strains that are epidemiologically unrelated [24]

Objectives

Methods

Results

Discussion

Conclusion