Amikacin and piperacillin/tazobactam are frequent antibiotic choices to treat bloodstream infection, which is commonly fatal and most often caused by bacteria from the family _Enterobacterales_. Here we show that two gene cassettes located …
Nitrofurantoin resistance in _Escherichia coli_ is primarily caused by mutations damaging two enzymes, NfsA and NfsB. Studies based on small isolate collections with defined nitrofurantoin MICs have found significant random genetic drift in _nfsA_ …
Increasing evidence suggests that microbial species have a strong within species genetic heterogeneity. This can be problematic for the analysis of prokaryote genomes, which commonly relies on a reference genome to guide the assembly process: any …
Little is known about the ecology of critically important antibiotic resistance among opportunistic human pathogens (e.g. _Escherichia coli_) on South American farms. By studying 70 farms in central-eastern Argentina, we identified that third-generation cephalosporin resistance (3GC-R) in _E. coli_ was mediated by mechanisms seen more often in certain species (pigs or dairy cattle) and that 3GC-R pig E. coli were more likely to be co-resistant to florfenicol and amoxicillin/clavulanate. This suggests that on-farm antibiotic usage is key to selecting the types of _E. coli_ present on these farms. 3GC-R E. coli were highly phylogenetically variable and we identified the de novo mobilisation of the resistance gene blaROB, alongside a novel florfenicol resistance gene, from pig pathogens into _E. coli_ on a mobile genetic element that was widespread in the study region. Overall, this shows the importance of surveying poorly studied regions for critically important antibiotic resistance which might impact human health.
Drug efficacy measured using pure cultures is not maintained in the presence of neighbouring microbes. Using simple physical laws, I pinpoint the mechanism for this change to demonstrate that drug efficacy can be predictably manupulated, and suggest why microbes began to co-operate and form communities.
The Mutant Selection Window (MSW) claims that selection for resistance begins only after the minimum inhibitory concentration, but there is no rationale behind it and no data to support it. Here we exposed *E. coli* to different antibiotic concentrations to measure which leads to fastest adaptation, and underpin the genetic mechanism.
For decades it was hypothesised that the growth rate of populations and their size engage in a trade-off, but the data was always inconclusive. Using bacteria, we set off to underpin a physical mechanism for this trade-off, and then explain why it is not always found in the data.
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Mathematically speaking, it is self-evident that the optimal control of complex, dynamical systems with many interacting components cannot be achieved with ‘non-responsive’ control strategies that are constant through time. Although there are notable …