In the decade since its discovery, has rapidly became a serious problem within healthcare environments. This fungal pathogen readily colonises skin and is responsible for numerous hospital outbreaks in different continents presenting high morbidity and mortality rates. However, the mechanisms it uses to spread throughout nosocomial settings still remains enigmatic. biofilm formation was monitored in real-time and the transcriptome of these biofilms were identified using RNA-sequencing and the ability of to persist on a polymer surface and tolerate treatment with a commonly used disinfectant in sodium hypochlorite (NaOCl) was assessed. Contrary to previous findings, biofilms were found to be heterogeneous and not dependent on cell phenotype. Through transcriptomic analysis and assigning transcripts into GO terms, a large number of genes involved in cell components, specifically fungal cell wall and cell membrane. Genes involved in these components were also up-regulated in dry biofilms of aggregating fungal cells compared to their single-cell counterparts. Aggregating biofilms were able to persist and tolerate disinfectant treatments more successfully than single-cell biofilms. These findings show that the aggregating phenotype of likely helps drive its survival and spread throughut hospital wards during outbreaks. Nonetheless there are still caveats in our understanding of biology and filling these holes will help in the development of more effective decontamination and infection control protocols for this emerging and deadly pathogen.

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