Antibiotic resistance in our pathogens is medicine’s climate change: caused by human activity, and resulting in more extreme outcomes. Resistance emerges in microbial populations when antibiotics act on phenotypic variance within the population. This can arise from either genotypic diversity (resulting from a mutation or horizontal gene transfer), or from differences in gene expression due to environmental variation, referred to as adaptive resistance. Adaptive changes can increase fitness allowing bacteria to survive at higher concentrations of antibiotics. They can also decrease fitness, potentially leading to selection for antibiotic resistance at lower concentrations. There are opportunities for other environmental stressors to promote antibiotic resistance in ways that are hard to predict using conventional assays. Exploiting our previous observation that commonly used herbicides can increase or decrease the minimum inhibitory concentration (MIC) of different antibiotics, we provide the first comprehensive test of the hypothesis that the rate of antibiotic resistance evolution under specified conditions can increase, regardless of whether a herbicide increases or decreases the antibiotic MIC. Short term evolution experiments were used for various herbicide and antibiotic combinations. We found conditions where acquired resistance arises more frequently regardless of whether the exogenous non-antibiotic agent increased or decreased antibiotic effectiveness. This is attributed to the effect of the herbicide on either MIC or the minimum selective concentration (MSC) of a paired antibiotic. The MSC is the lowest concentration of antibiotic at which the fitness of individuals varies because of the antibiotic, and is lower than MIC. Our results suggest that additional environmental factors influencing competition between bacteria could enhance the ability of antibiotics to select antibiotic resistance. Our work demonstrates that bacteria may acquire antibiotic resistance in the environment at rates substantially faster than predicted from laboratory conditions.
Baseline studies are needed to identify environmental reservoirs of non-pathogenic but associating microbiota or pathogenic bacteria that are resistant to antibiotics and to inform safe use of freshwater ecosystems in urban and agricultural settings. Mesophilic bacteria and Escherichia coli were quantified and isolated from water and sediments of two rivers, one in an urban and one in an agricultural area near Christchurch, New Zealand. Resistance of E. coli to one or more of nine different antibiotics was determined. Additionally, selected strains were tested for conjugative transfer of resistances. Despite having similar concentrations of mesophilic bacteria and E. coli, the rivers differed in numbers of antibiotic-resistant E. coli isolates. Fully antibiotic-susceptible and -resistant strains coexist in the two freshwater ecosystems. This study was the first phase of antibiotic resistance profiling in an urban setting and an intensifying dairy agroecosystem. Antibiotic-resistant E. coli may pose different ingestion and contact risks than do susceptible E. coli. This difference cannot be seen in population counts alone. This is an important finding for human health assessments of freshwater systems, particularly where recreational uses occur downstream.
Antibiotic resistance is medicine's climate change: caused by human activity, and resulting in more extreme outcomes. Resistance emerges in microbial populations when antibiotics act on phenotypic variance within the population. This can arise from either genotypic diversity (resulting from a mutation or horizontal gene transfer), or from 'adaptive' differences in gene expression due to environmental variation. Adaptive changes can increase fitness allowing bacteria to survive at higher concentrations of the antibiotic.They can also decrease fitness, potentially leading to selection for antibiotic resistance at lower concentrations. There are opportunities for other environmental stressors to promote antibiotic resistance in ways that are hard to predict using conventional assays.Exploiting our observation that commonly used herbicides can increase or decrease the minimum inhibitory concentration (MIC) of different antibiotics, we provide the first comprehensive test of the hypothesis that the rate of antibiotic resistance evolution under specified conditions can increase, regardless of whether a herbicide increases or decreases the antibiotic MIC. Short term evolution experiments were used for various herbicide and antibiotic combinations. We found conditions where acquired resistance arises more frequently regardless of whether the exogenous non-antibiotic agent increased or decreased antibiotic effectiveness. This "damned if you do/damned if you don't" outcome suggests that the emergence of antibiotic resistance is exacerbated by additional environmental factors that influence competition between bacteria. Our work demonstrates that bacteria may acquire antibiotic resistance in the environment at rates substantially faster than predicted from laboratory conditions. 24 (resulting from a mutation or horizontal gene transfer), or from 'adaptive' differences in gene 25 expression due to environmental variation. Adaptive changes can increase fitness allowing 26 bacteria to survive at higher concentrations of the antibiotic. They can also decrease fitness, 27 potentially leading to selection for antibiotic resistance at lower concentrations. There are 28 opportunities for other environmental stressors to promote antibiotic resistance in ways that are 29 hard to predict using conventional assays. Exploiting our observation that commonly used 30 herbicides can increase or decrease the minimum inhibitory concentration (MIC) of different 31 antibiotics, we provide the first comprehensive test of the hypothesis that the rate of antibiotic 32 resistance evolution under specified conditions can increase, regardless of whether a herbicide 33 increases or decreases the antibiotic MIC. Short term evolution experiments were used for 34 various herbicide and antibiotic combinations. We found conditions where acquired resistance 35 arises more frequently regardless of whether the exogenous non-antibiotic agent increased or 36 decreased antibiotic effectiveness. This "damned if you do/damned if you don't" outcome 37 suggests tha...
We report the draft genomes of 15 multidrug-resistant and potentially pathogenic Escherichia coli strains isolated from watercress, cockles, or the surrounding water in Aotearoa, New Zealand.
Antibiotic resistance is medicine's climate change: caused by human activity, and resulting in more extreme outcomes. Resistance emerges in microbial populations when antibiotics act on phenotypic variance within the population. This can arise from either genotypic diversity (resulting from a mutation or horizontal gene transfer), or from 'adaptive' differences in gene expression due to environmental variation. Adaptive changes can increase fitness allowing bacteria to survive at higher concentrations of the antibiotic.They can also decrease fitness, potentially leading to selection for antibiotic resistance at lower concentrations. There are opportunities for other environmental stressors to promote antibiotic resistance in ways that are hard to predict using conventional assays.Exploiting our observation that commonly used herbicides can increase or decrease the minimum inhibitory concentration (MIC) of different antibiotics, we provide the first comprehensive test of the hypothesis that the rate of antibiotic resistance evolution under specified conditions can increase, regardless of whether a herbicide increases or decreases the antibiotic MIC. Short term evolution experiments were used for various herbicide and antibiotic combinations. We found conditions where acquired resistance arises more frequently regardless of whether the exogenous non-antibiotic agent increased or decreased antibiotic effectiveness. This "damned if you do/damned if you don't" outcome suggests that the emergence of antibiotic resistance is exacerbated by additional environmental factors that influence competition between bacteria. Our work demonstrates that bacteria may acquire antibiotic resistance in the environment at rates substantially faster than predicted from laboratory conditions. 24 (resulting from a mutation or horizontal gene transfer), or from 'adaptive' differences in gene 25 expression due to environmental variation. Adaptive changes can increase fitness allowing 26 bacteria to survive at higher concentrations of the antibiotic. They can also decrease fitness, 27 potentially leading to selection for antibiotic resistance at lower concentrations. There are 28 opportunities for other environmental stressors to promote antibiotic resistance in ways that are 29 hard to predict using conventional assays. Exploiting our observation that commonly used 30 herbicides can increase or decrease the minimum inhibitory concentration (MIC) of different 31 antibiotics, we provide the first comprehensive test of the hypothesis that the rate of antibiotic 32 resistance evolution under specified conditions can increase, regardless of whether a herbicide 33 increases or decreases the antibiotic MIC. Short term evolution experiments were used for 34 various herbicide and antibiotic combinations. We found conditions where acquired resistance 35 arises more frequently regardless of whether the exogenous non-antibiotic agent increased or 36 decreased antibiotic effectiveness. This "damned if you do/damned if you don't" outcome 37 suggests tha...
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