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E. coli outbreak strain in genome race

Sequence data reveal pathogen's deadly origins.

The collaborative atmosphere that surrounded the public release of genome sequences in the early weeks of this year's European Escherichia coli outbreak has turned into a race for peer-reviewed publication.

A paper published in PLoS One today, by Dag Harmsen from the University of Münster, Germany, and his colleagues, contains the first comparative analysis of the sequence of this year's E. coli outbreak strain (called LB226692 in the publication) and a German isolate from 2001 (called 01-09591), which was held by the E. coli reference laboratory at the University of Münster, headed by Helge Karch. The scientists also compared the two strains with the publicly available genome of strain 55989, isolated in central Africa in the 1990s.

The LB226692 and 01-09591 genomes were sequenced using an Ion Torrent PGM sequencer from Life Technologies of Carlsbad, California (see 'Chip chips away at the cost of a genome'). The authors say that their publication is the first example of next-generation, whole-genome sequencing being used for real-time outbreak analysis. "This represents the birth of a new discipline — prospective genomics epidemiology," says Harmsen. He predicts that this method will rapidly become routine public-health practice for outbreak surveillance.

But Harmsen's group was pipped to the publishing post by Rolf Daniel and his colleagues at the University of Göttingen in Germany, who published a comparison of the sequence of two isolates from the outbreak with the 55989 strain in Archives of Microbiology on 28 June. Harmsen says that this competition is why his group did not release the 2001 strain sequence before today's PLoS One publication.

Both groups say that their genomic sequencing and analysis were conducted independently. But their findings don't really differ from sequence analyses that other scientists were simultaneously documenting in the public domain, following the release, on 2 June, by China's BGI (formerly known as the Beijing Genomics Institute) of a full genome sequence of the outbreak strain — also generated using Ion Torrent sequencing. These scientists say that there is very little information in either publication that was not previously available on their website. "The crowd-sourcing efforts arrived at almost all of the scientific conclusions about the strain comparisons first," says Mark Pallen from the University of Birmingham, UK, "so we're surprised and disappointed that these findings are not referred to in these papers."

Everyone agrees that the Münster laboratory released information on defining genetic features of the 2011 outbreak strain that allowed accurate patient diagnosis and strain tracking as soon as they had the information. The current squabbling revolves around genomic details that point to how the unusual strain evolved.

So what have the combined analyses revealed so far? All of the strains have a similar enteroaggregative E. coli (EAEC) genetic background, but the 2011 outbreak strain contains plasmid- and chromosome-encoded genes that differ both from the 2001 German and from the earlier African strain. The 2011 and 2001 strains, but not the African strain, carry the important stx gene for Shiga-toxin production — the cause of so many people's sickness — although the African strain carries an intact stx integration site, suggesting it may have evolved from a strain that did once carry it. The African strain also does not contain a tellurite-resistance gene that the other two strains do. The 2011 and 2001 also have different genes for fimbriae — the cell protrusions that make EAEC bacteria particularly sticky.

The authors of the paper in PLoS One hypothesize that the strains all derive from a common Shiga-toxin producing EAEC progenitor. They say the genetic steps between the three strains are suggestive of a 'common ancestor model'. It is evolutionarily more likely that bacteria lose genetic elements than gain them, and Harmsen cites the large ter genetic island as an example of a genetic element more likely to have been lost from a common progenitor than gained by subsequently appearing strains.

"All of these analyses are an example of bacterial evolution being in constant flux," says Pallen, reiterating that this outbreak highlighted the importance of establishing more flexible diagnostic frameworks for E. coli strains.

Harmsen says he expects at least two further papers on analysis of the genome sequences to be published by independent groups in the next few weeks.

Credit: Manfred Rohde, Helmholtz-Zentrum für Infektionsforschung (HZI)

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This story has been cross-posted from Nature's news blog.

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Turner, M. E. coli outbreak strain in genome race. Nature (2011).

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