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Rapid colonisation of environmental plastic waste by pathogenic bacteria drives adaptive phenotypic changes
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This study showed that pathogenic E. coli O157 can colonize plastic surfaces within 30 minutes and persist for at least 21 days at concentrations sufficient to cause human infection under simulated environmental conditions. Repeated colonization and dissociation cycles enhanced E. coli O157 biofilm formation and antibiotic tolerance, suggesting that plastic pollution may be selecting for more virulent and persistent pathogen variants in the environment.
Microbial biofilms on environmental plastic pollution can serve as a reservoir for both pathogenic and commensal bacteria. Associating with this 'plastisphere', provides a mechanism for the wider dissemination of pathogens within the environment and a greater potential for human exposure. For pathogens to bind to environmental plastic waste they need to be in close contact with it; therefore, understanding how rapidly pathogens can bind to plastics and the temporal colonisation dynamics of the continual cycling between the plastisphere and the environment are important factors for quantifying the persistence of human pathogens. Using simulated environmental conditions, we demonstrate that pathogenic E. coli O157 can rapidly colonise plastics (within 30 min) and persist for extended periods (at least 21 days), at concentrations sufficient to cause human infection. Importantly, repeated colonisation and dissociation cycles of E. coli O157 from the plastisphere leads to an enhanced capacity for persistence and the emergence of variants with increased virulence traits, including improved biofilm formation and antibiotic tolerance. This phenotypic adaptation to repeated colonisation of environmental plastic surfaces could be selecting for more persistent and virulent strains of pathogens, and hence increase the co-pollutant risks associated with plastic pollution.
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