Abstract
BackgroundStrains of Escherichia coli cause a wide variety of intestinal and extra-intestinal diseases in both humans and animals, and are also often found in healthy individuals or the environment. Broadly, a strong phylogenetic relationship exists that distinguishes most E. coli causing intestinal disease from those that cause extra-intestinal disease, however, isolates within a recently described subclass of Extra-Intestinal Pathogenic E. coli (ExPEC), termed endometrial pathogenic E. coli, tend to be phylogenetically distant from the vast majority of characterised ExPECs, and more closely related to human intestinal pathogens. In this work, we investigate the genetic basis for ExPEC infection in the prototypic endometrial pathogenic E. coli strain MS499.ResultsBy investigating the genome of MS499 in comparison with a range of other E. coli sequences, we have discovered that this bacterium has acquired substantial lengths of DNA which encode factors more usually associated with ExPECs and less frequently found in the phylogroup relatives of MS499. Many of these acquired factors, including several iron acquisition systems and a virulence plasmid similar to that found in several ExPECs such as APEC O1 and the neonatal meningitis E. coli S88, play characterised roles in a variety of typical ExPEC infections and appear to have been acquired recently by the evolutionary lineage leading to MS499.ConclusionsTaking advantage of the phylogenetic relationship we describe between MS499 and several other closely related E. coli isolates from across the globe, we propose a step-wise evolution of a novel clade of sequence type 453 ExPECs within phylogroup B1, involving the recruitment of ExPEC virulence factors into the genome of an ancestrally non-extraintestinal E. coli, which has repurposed this lineage with the capacity to cause extraintestinal disease. These data reveal the genetic components which may be involved in this phenotype switching, and argue that horizontal gene exchange may be a key factor in the emergence of novel lineages of ExPECs.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1075) contains supplementary material, which is available to authorized users.
Highlights
Strains of Escherichia coli cause a wide variety of intestinal and extra-intestinal diseases in both humans and animals, and are often found in healthy individuals or the environment
We suggest that this ExPECassociated DNA within the genome of MS499 has been horizontally acquired during its recent evolutionary history, and we speculate that the recruitment of this DNA into the MS499 genome has expanded the niche of this isolate, and allows it to cause extraintestinal disease
In light of the ability for MS499 to cause extraintestinal disease in animals, we investigated whether E. coli similar to MS499 had been isolated from other extraintestinal infections
Summary
Strains of Escherichia coli cause a wide variety of intestinal and extra-intestinal diseases in both humans and animals, and are often found in healthy individuals or the environment. Most E. coli isolates can be grouped into 7 broad phylogroups, termed A, B1, B2, C, D, E and F, based on the distribution of a number of target genes and multilocus sequencing typing (MLST) methods [1] Dispersed across these phylogroups are several pathotypes, including extraintestinal pathogenic E. coli (ExPEC) such as uropathogenic (UPEC) and neonatal meningitis-associated (NMEC), and intestinal pathogenic E. coli (IPEC) including enterohaemorrhagic (EHEC), enteropathogenic (EPEC), and enterotoxigenic (ETEC) strains. Counter-intuitively, E. coli from classical ExPEC groups are frequently isolated as human intestinal commensals, and successfully compete with resident intestinal microflora to colonise the human gut in the absence of gastro-intestinal disease [17,18] They may constitute the predominant faecal commensal E. coli type in a significant proportion of healthy humans [2,17], and many of the PAIs which impact on ExPEC disease function as intestinal colonisation fitness factors [19,20,21]
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