Professor Jodi Lindsay’s genomic studies are providing novel insights into DNA transfer in methicillin-resistant Staphylococcus aureus (MRSA), and how it adapts to hospital environments.
Following a peak in the 2000s, the prevalence of MRSA in UK hospitals has declined markedly. As well as studies on plasmid transfer in MRSA, Professor Jodi Lindsay has uncovered a likely reason for this decline.
Having helped to sequence the first MRSA genome, Professor Lindsay has gone on to identify a critical mechanism limiting the spread of antimicrobial resistance genes via plasmids and other genetic elements. While plasmids containing resistance genes are readily shared within an MRSA clonal group during colonisation, they are rarely transmitted between them. The reason, Professor Lindsay discovered, is the strain specificity of the Sau1 system, part of MRSA’s defence against phage, which targets ‘foreign’ plasmids for destruction.
Were it not for this mechanism, multidrug-resistant MRSA might be an even bigger healthcare problem. However, some plasmids lack Sau1 target sites, enabling them to be shared more widely, despite plasmid exchange may be more common than previously thought. However, strains that have acquired plasmids tend not to persist, probably because they are out-competed by existing strains – emphasising the importance of selective pressures in microbial survival.
These findings are supported by Professor Lindsay’s clinically oriented research. An analysis of ten years’ MRSA data from St George’s Hospital pointed to changing prescription practice, rather than screening or better infection control, as the key factor behind the decline in MRSA. Reduced use of fluoroquinolones, to minimise Clostridium difficile infections, may also have removed a selective pressure that previously favoured the growth of fluoroquinolone-resistant MRSA.