Digital Public Defence: Silje Nøstvedt Ramstad
MSc Silje Nøstvedt Ramstad at Institute of Clinical Medicine will be defending the thesis “Shiga toxin-producing Escherichia coli – aspects of their pathogenicity and effects of antimicrobials” for the degree of PhD (Philosophiae Doctor).
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture – time and place
- First opponent: Reader Heather Allison, University of Liverpool, UK
- Second opponent: Head of Centre Flemming Scheutz, Statens Serum Institut, Denmark
- Third member and chair of the evaluation committee: Professor II Anna Kristina Bjerre, University of Oslo
Chair of the Defence
Associate Professor Dag Henrik Reikvam, University of Oslo
Senior Scientist Lin Cathrine Thorstensen Brandal, Norwegian Institute of Public Health
Shiga toxin-producing Escherichia coli (STEC) is a foodborne pathogen. The clinical picture ranges from asymptomatic to bloody diarrhea, and in about 5% of cases the severe complication haemolytic uremic syndrome (HUS) develops. The key virulence factor is the Shiga toxin (Stx), which is encoded on bacteriophages incorporated into the bacterial genome. STEC with Stx subtypes Stx2a, Stx2c and/or Stx2d are classified as high-virulent. Current clinical guidelines advice against the use of antimicrobials, as some studies have shown that it may increase the production of Stx and worsen disease outcome.
The main aim of this study was to elucidate different characteristics of high virulent STEC to explore the possibility of antimicrobial treatment of STEC infections. Antimicrobial exposure experiments revealed that meropenem, gentamicin and azithromycin did not increase Stx production in high virulent STEC in vitro. A study of the prevalence of genotypic antimicrobial resistance in STEC showed that 16% of clinical STEC harboured known genotypic resistance markers against antimicrobials. A characterization of Stx2a phages of O145:H25 STEC, which is highly associated with HUS in Norway, demonstrated that these phages were conserved and shared integration site with the remnants of another phage (shadow-phage). An additive effect of virulence genes from the Stx2a phage and the shadow-phage might be associated with the increased pathogenicity seen in these STEC.
Overall, our results indicate that some classes of antimicrobials may be candidates for treatment of high virulent STEC infections. Furthermore, the interaction between different bacteriophages of STEC might increase the pathogenicity of the bacterium.
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