Dr Claire Turner

Room: F15b
0114 222 2819


Career History

  • 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.

Research Keywords

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


 My 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.


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).

PhD Opportunities

If you interested in joining the group then please contact me directly by email at c.e.turner@sheffield.ac.uk.

I have a FULLY FUNDED PhD studentship, available to home, EU or international students. If you wish to self fund a PhD then please contact me directly to discuss potential projects.

Enhancing the activity of existing antibiotics on persistent Streptococcal infections by targeting amyloid components of biofilm - FULLY FUNDED

Group A Streptococcus (GAS) is a human pathogen that primarily infects the skin and oropharynx where it can lead to severe or lethal infections (necrotising fasciitis). Despite their sensitivity to penicillin, treatment failure and recurrent infections are common and aggressive surgical debridement is often the only treatment for deep tissue infections. Biofilm-like formation by GAS, either on mucosal surfaces such as the tonsil or during deep tissue infections may shield against antimicrobials, reducing drug penetrance.

The aim of this project is to characterise a GAS surface adhesion factor, Asp as an amyloid former, using recombinant expression to produce an in vitro model for structural/mechanistic studies using high-resolution electron microscopy. Validation in situ will be done by targeted mutagenesis of Asp in GAS, and heterologous expression of Asp in Lactococcus lactis. The contribution of amyloids to biofilm/adherence of GAS to surfaces and cell lines, including pharyngeal cells, will be measured. We will assess the efficacy of multidrug treatment of GAS by combining antimicrobials with amyloid modifiers.

This project is a new approach to understanding the mechanisms by which this important pathogen causes disease and, crucially how it can resist treatment during infection. We will identify new intervention strategies to stop the spread of GAS and the severity of infection. The combination of biophysical/mechanistic studies with high resolution electron microscopy studies on the recombinant protein together with direct observation in cell culture will result in a substantial advance in our understanding of these processes and provide a unique inter-disciplinary training opportunity.

Please contact me (c.e.turner@sheffield.ac.uk) or co-supervisor Dr Rosie Staniforth (r.a.staniforth@sheffield.ac.uk) for more information.

The studentship is funded by the Florey Institute and Imagine:Imaging Life. It provides full tuition fees (UK, EU or Overseas); and an annual, tax-free maintenance stipend at the standard RCUK rate, for up to 3.5 years full-time study, subject to satisfactory progress. You should have, or expect to achieve, a first or upper second class UK honours degree or equivalent, in a relevant area (e.g. Biology, Molecular Biosciences, Biophysics, Biochemistry).  Anticipated start date October 2017. The closing date for applications is Feb 28 2017.

Applying :Scholarships are awarded on a competitive basis - applications are assessed on the basis of academic success and qualifications, experience, research background and a clear and well-articulated reason for being considered. For information on applying, please see https://www.sheffield.ac.uk/postgraduate/research/apply/applying.

Journal articles


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