Antimicrobial resistance (AMR) threatens almost the entirety of our healthcare system if we are no longer able to treat common infections, provide post-operative care or protect patients with chronic health conditions. The immediate priority is better antibiotic stewardship and individualised therapy to target the right antimicrobial at the right dose to the right patient. Doing so would be both clinically effective for the patienthelp prevent evolution of drug resistance in the community.
This project will use new omic methods to understand the biology of antimicrobial resistance and underpin new methods of individualised antimicrobial therapy. The project will study clinical samples of Gram-negative bacteria, such as Pseudomonas aeruginosa, from hospitals and large clinical trials where resistance has emerged. We want to be able to predict which infections will develop resistance and which remain susceptible to therapy The genome of the pathogen is likely to affect its ability to evolve resistance and you will investigate genomic features that may enable this. This may include the content of genes carried by a pathogen and hence its ability to metabolise or excrete antibiotics. To test this you will use mass spectrometry-based metabolomics to investigate the range and dynamics of metabolites produced by drug sensitive and resistant pathogens.
Your project will involve both wet-lab and computational analysis. You will be trained in microbiology, genomics and metabolomics, and the analysis of complex datasets that combine omic data, drug resistance phenotypes and clinical data. You will learn experimental design and the application of biological theory to real-world clinical problems. Training will be through formal courses, guided laboratory work and analyses, and through being part of large, vibrant research groups.
This project would suit someone with an interest in fundamental biology that addresses medical problems, and who wishes to develop critical thinking through a PhD.
To apply for this opportunity, please send your CV and 2 references to firstname.lastname@example.org.
This opportunity will close once a suitable candidate has been found.
Open to EU/UK applicants
Details of costs can be found on the University website: https://www.liverpool.ac.uk/study/postgraduate-research/fees-and-funding/fees-and-costs/
Williams, D., Fothergill, J. L., Evans, B., Caples, J., Haldenby, S., Walshaw, M. J., . . . Paterson, S. (2018). Transmission and lineage displacement drive rapid population genomic flux in cystic fibrosis airway infections of a Pseudomonas aeruginosa epidemic strain. MICROBIAL GENOMICS, 4(3). doi:10.1099/mgen.0.000167
Williams, D., Evans, B., Haldenby, S., Walshaw, M. J., Brockhurst, M. A., Winstanley, C., & Paterson, S. (2015). Divergent, Coexisting Pseudomonas aeruginosa Lineages in Chronic Cystic Fibrosis Lung Infections. American Journal of Respiratory and Critical Care Medicine, 191(7), 775-785. doi:10.1164/rccm.201409-1646OC
AlRabiah, H., Allwood, J.W., Correa, E., Xu, Y. & Goodacre, R. (2018) pH plays a role in the mode of action of trimethoprim on Escherichia coli. PLoS ONE 13: e0200272