Investigating the transition of Staphylococcus aureus from commensal to pathogen
Virulence is a key driver of a pathogen’s ability to cause disease. It encompasses various aspects of infection, including initial colonisation of a host, evasion of the immune system and invasion of tissues and organs. My research started with a focus on the genetic basis of virulence factor production, specifically toxins, in the opportunistic pathogens Staphylococcus aureus (DOI: 10.1038/s41598-017-14110-8) and Streptococcus pneumoniae (DOI: 10.1099/mgen.0.000784). Both are medically important pathogens, causing a range of diseases from mild skin and upper respiratory tract infections to life threatening septicaemia and pneumonia. Using functional genomics, I identified novel genes which contribute to toxin production in these species.
Following this, I began studying the evolutionary dynamics of pathogen virulence, with a focus on how host microbiota might drive changes in virulence evolution. Using a C. elegans nematode worm model of invasive S. aureus infection, I have characterised how competitive interactions between S. aureus and a native host microbiota community affect pathogen virulence over evolutionary time.
My current work focuses on the transition of opportunistic pathogens from asymptomatic colonisers of the human nasopharynx to invasive pathogens. I am particularly interested in characterising in more detail the interactions between these opportunists and host microbiota communities, to better understand the context in which the transition to pathogenesis takes place.