Methicillin-resistant Staphylococcus aureus (MRSA) continues to be a formidable pathogen in clinical and community settings. Capitalising on a multitude of virulence factors which enable a diverse and complex disease profile, while still ensuing survival though non-pathogenic colonisation, it remains a critical contributor to the burden of infection in Australian hospitals. The heterogeneity of antibiotic resistance profiles between MRSA clones and the seemingly counterintuitive re-emergence of gentamicin susceptible MRSA (GS-MRSA) cannot be accounted for by changing patterns of antimicrobial use alone. Furthermore, the replacement of gentamicin resistant strains (GR-MRSA) by gentamicin susceptible strains (GS-MRSA) suggests clonal displacement may be the result of a direct interaction between organisms.

 Previous studies have explored MRSA co-culture in broth, demonstrating that one clone ultimately out-competes the other for nutrients and growth factors. This study provides further explanation for MRSA clonal displacement, demonstrating a direct and aggressive inhibition of GR-MRSA by GS-MRSA. Isolates were collected from John Hunter hospital between 2000 and 2014 and selected based on their antibiotic susceptibility profiles. Utilising a variation of agar-overlay culture, GS-MRSA has been shown not only to out compete GR-MRSA but to directly inhibit its growth through a seemingly bactericidal mode of action. This has been shown to occur not only in large concentrations, but also in cultures where CFUs present are reflective of a clinical burden of nasal colonisation or disease. This phenotypic model was then correlated with sequence data obtained from next generation sequencing with the aim of typing clones and identifying variation at the nucleotide level that may elucidate the mechanism behind bactericidal activity observed in culture. These findings offer novel insight into MRSA clonal interactions and raise questions pertaining to our ideas of fitness in relation to microbial evolution.