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Sometimes a paper comes along which is simply too good not to include in a journal club. An exciting yet contentious  finding that presents as a paradigm shift in our understanding of a pathogenic microbe with far reaching implications for public health.

Unfortunately I just couldn’t shift my focus to that paper from one essentially about toilets. This weeks paper therefore concerns that which we would rather not know – the diversity, and sources, of surface microbial communities in public restrooms.

The authors present the application of 16S rRNA sequence analysis (apologies, it is another next-gen approach) to further our understanding of microbial communities on surfaces.  They in turn demonstrate the utility of SourceTracker (a Bayesian-based comparison tool) for elucidating the likely source of these contaminations. The implications of their findings to human health are finally discussed.

Some points to consider:

1. Was it really worth it?

2. Was the goal of this study  clear?

3. Given the analysis methods employed can any extrapolation to the prevalence of disease causing bacteria really be made?

As ever please feel free to leave further discussion points……


Bit of a delayed transcript for this session I’m afraid because of conferences/friend’s wedding/jet lag!

I’ve not had time to create the transcript here directly but there is a storified version.

Thanks everyone who took part – I know there were a lot of other things competing for your time (not least the England match!)

Looking forwards to seeing you all next time 🙂

Zoonotica here posting on behalf of @flashton2003 the summary and discussion points for the next #microtwjc on Tues 19th June at 8pm BST.

The paper we’ll be discussing is:

Hfq virulence regulation in enterohemorrhagic Escherichia coli O157:h7 strain 86-24, Kendall et al., J. Bac., v193, p6843, 2011

The authors examined the role of the small RNA chaperone Hfq in the regulation of virulence in Enterohemorrhagic Escherichia coli O157:H7 (EHEC). They found that the deletion of hfq down regulated the transcriptional activator of a pathogenicity associated locus (locus of enterocyte effacement, LEE) as well as a two component system (qseBC) which is involved in interkingdom signalling and virulence gene regulation (it upregulates shiga toxin production) in EHEC. They also examined the production of shiga toxin protein and the virulence of the mutant in a cell model and found both to be decreased. The author’s findings differ from work done on another EHEC strain in which deletion of hfq led to the upregulation of virulence genes. They ascribe this difference to the different genetic background of the two strains which have each acquired the virulence genes by horizontal gene transfer.

Discussion points

* How do you think that the thoroughness and technical aspects of this work compared with the previous work on the related strain which showed that deletion of hfq increase the production of various virulence associated proteins?

* What experiments could be performed to elucidate the different roles of Hfq in the different strains?

* Interesting that strains which exhibit such similar phenotypes (i.e. EHEC) have such different ways of regulating the genes which result in this phenotype. What evolutionary mechanism could explain this?

* What other interesting phenotypes are associated with post-transcriptional regulation by e.g. Hfq?

As ever please feel free to leave any other discussion points below, plus if any of you write/have written a blog post on the paper please feel free to plug that below too. 🙂

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