Molecular mechanisms underpinning intraspecies co-infections with multiple <i>Acinetobacter baumannii</i> strains

<p><em>Acinetobacter baumannii </em>is one of the leading causes of infections worldwide. The ubiquity of this pathogen within healthcare facilities have led to previous reports of <em>A. baumannii </em>being implicated in co-infections with other hospital-associated bacteria. Thus, we hypothesise that intraspecies co-infections involving multiple strains of <em>A. baumannii </em>occur in patients over time but are underreported due to the technical difficulty of resolving similar bacterial strains using standard molecular techniques. Consequently, comprehensive molecular information on intraspecies interactions is severely lacking. In this project, I investigated a critical research gap regarding whether different co-infecting <em>A. baumannii </em>strains are cooperative or antagonistic partners that potentiate or attenuate each other’s virulence and resistance to external stresses like antibiotics. The genome-wide screening technique of transposon-directed insertion site sequencing (TraDIS) was employed to screen for the molecular drivers of intraspecies interactions, by competing a dense <em>A. baumannii </em>ATCC 17978 TraDIS mutant library against a range of other <em>A. baumannii </em>strains – including pathogenic (AB5075_UW, BAL062) and environmental (E-072658) isolates. This approach identified a range of conditionally important genes mediating the fitness of ATCC 17978 in intraspecies co-culture, including known mediators of interbacterial interactions as well as several novel community-dependent fitness determinants.</p>