About this Research Topic
Here, we discuss these “knock-on” effects that are evident throughout various parts of the cell across a number of bacterial species. Various cell morphology changes can be observed in response to antibiotic exposure, including persister cell formation, associated decreased cellular metabolism, smaller cell size, and even transformation to different cellular states, like the switching to L-forms/cell-wall deficient (CWD) bacteria in response to Beta-lactam treatment. Other downstream effects include alterations of the levels of virulence and pathogenicity after antibiotic treatment, which is especially worrying in hospital-associated pathogenic bacteria. Sub-inhibitory concentrations of antibiotic exposure can also lead to increased biofilm formation. Antibiotic exposure often results in the activation of mobile genetic elements, induction of latent viruses, and movement of antibiotic genes. Further, alteration of metal ion homeostasis and lipid composition of the cells occurs. Lastly, the antibiotics themselves can act in other roles beyond killing, for example, antibiotics at low concentrations can act directly as signaling molecules and feed into communication pathways and microbial community coordination. Overall, these reported effects likely only represent the tip of the iceberg in our understanding of the secondary effects of antibiotics on bacterial cells. Future research will allow us to fully comprehend the overall implications of antibiotic treatment.
This Research Topic focuses on these secondary effects of antibiotics to explore the diverse ways that human use of these important compounds is impacting the physiology, behavior, and evolution of bacteria.
Keywords: antibiotic resistance, antimicrobials, genetics
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