CTurnerDr Claire Turner

Research Fellow

Room: F15b
Tel: 0114 222 2819
Email: c.e.turner@sheffield.ac.uk

Research

Research Precis

fig1My research focus is on trying to understand the mechanisms behind upsurges in disease caused by the human pathogen Streptococcus pyogenes (also known as group A Streptococcus). Upsurges occur frequently and can be associated with specific genotypes. I use a combination of whole genome sequencing, epidemiology, clinical analysis and phenotypic work to try and identify what makes strains successful at causing disease and become suddenly more abundant.
One of my particular interests is recombination-related genome remodelling, which we identified to be the driving force behind a very recent shift in the population of the S. pyogenes genotype emm89. A new variant of emm89 emerged from the population having undergone six regions of recombination within the core genome. This recombination-related genome remodelling led to substantial phenotype changes, including loss of the hyaluronic acid capsule and increase of toxin expression, altering the way this genotype interacted with the host. The emergent variant has now become the dominant form of emm89 in the UK and globally, causing a high level of disease. Understanding how recombination occurs and what the impact of recombination is on the bacterium are part of my research aims.

Figure 1. Whole genome sequencing of 131 isolates of emm89 S. pyogenes from the UK identified an emergent clade variant that differed from the rest of the population of emm89 S. pyogenes by a high number of SNPs. This high level of variation is unexpected within a genotype but, importantly, the majority of the SNPs actually clustered in to six regions within the genome, which is indicative of recombination.

fig2

Figure 2. (A) The largest region of recombination with emm89 encompassed the toxin genes nga and slo, which encode for NADase and Streptolysin O, and when combined can be lethal to host cells. These toxins are also thought to promote survival of S. pyogenes inside host cells. Compared to the previous variant, this region in the emergent variant contained a high number of SNPs (indicated by vertical lines; black = synonymous, red = non-synonymous) indicating that this region had been obtained from an external donor. (B) The expression of nga was high in the emergent variant (red) compared to nearly undetectable levels in the previous emm89 variant (blue).

Research Keywords

Microbiology, Streptococcus pyogenes, Group A streptococcus, bacterial evolution, scarlet fever, necrotising fasciitis, tonsilitis, whole genome sequencing, recombination.

Teaching
Career History

Career History

  • 2017-present: Florey Institute Research Fellow, University of Sheffield
  • 2013-2016: Imperial College Junior Research Fellow
  • 2009-2013: Research Associate, National Centre for Infection Prevention & Management, Imperial College London
  • 2005-2009: PhD, Imperial College London.



Journal articles

Chapters

  • Efstratiou A, Lamagni T & Turner CE (2016) Streptococci and Enterococci In Cohen J, Powderly W & Opal S (Ed.), Infectious Diseases 4th edition Elsevier