Dr Rachel Floyd BSc Hons, PhD

Urinary tract infections (UTI) are among the most common infections seen in primary care and account for 40% of all hospital-aquired infections. In uncomplicated UTI, Escherichia coli is the primary causative agent responsible for up to 80% of cases with Klebsiella pneumoniae and Pseudomonas aeruginosa being less frequently detected (7-15%). However, complicated UTI are more frequently caused by Pseudomonas aeruginosa, which shows a higher prevalence of antimicrobial resistance and greater propensity to form biofilms on medical devices. The pathogenesis of uropathogenic Escherichia coli (UPEC)-mediated UTI has been extensively characterized, but there is still much we do not understand about the interplay between bacteria and host factors found in the urinary tract. Our group is studying many aspects of UTIs including bacterial virulence in disease, host response, and prevalence of antimicrobial resistance using molecular microbiology, cell biology and physiology and real-time live cell imaging techniques.

Collaborators: Professor Craig Winstanley, Professor Jay Hinton, Dr Disa Hammarlof, Dr Carsten Kroger

Urinary tract infection (UTI) remains a common but widely misunderstood infectious disease. Most UTI are caused by Escherichia coli colonization of the urethra and ascension into the bladder causing cystitis. Pyelonephritis can develop as a consequence of bacteria ascending the ureters leading to kidney scarring and kidney failure. Efficient peristalsis is therefore vital in maintaining renal health. E. coli colonization can impair ureteric contractility and cause dilation which in turn potentiates infection due to urinary stasis and/or vesicoureteric reflux but little is known about the mechanisms of impaired function.
Our aim to elucidate whether the phenotypic effects of UPEC on ureteric contractility correlate with virulence factor expression using a combination of bacterial genomics and intact tissue modelling.

Collaborators: Professor Craig Winstanley, Dr Mat Upton, Dr Roy Chaudhuri

Urinary tract infections are widespread in the general population and also account for 20% of all hospital acquired infections. Most of these infections are caused by E. coli but a small proportion are caused by Pseudomonas aeruginosa bacteria which are more likely to be resistant to antibiotics, thus making the infections more difficult to treat. Pseudomonas aeruginosa are able to survive for extended periods of time on hard surfaces and medical devices such as catheters by forming protective structures called biofilms. Despite the prevalence of UTI infections, we understand very little about the driving forces that initiate this adaptation and trigger biofilm formation in Pseudomonas aeruginosa in urinary tract infections. Studies suggest that hormones such as oestrogen may play a key role in triggering modifications in the behaviour and characteristics of Pseudomonas bacteria which enable them to survive and cause disease. This work uses a combination of molecular microbiology, cell biology and real-time live cell imaging to investigate whether hormones can drive adaptation in clinical isolates of Pseudomonas aeruginosa in different model systems.

Collaborators: Dr Jo Fothergill