Mechanism and Evolution of Antibiotic Resistance

Because of the continued process of evolution and natural selection with antimicrobials, bacterial pathogens are gaining the edge over human ingenuity and our collective ability to produce new antimicrobials and utilize existing antimicrobials wisely. While mechanisms of bacterial antibiotic resistance vary in their mechanics and genetic underpinnings, all mechanisms of resistance essentially disallow antimicrobials from reaching their specific target or targets. Over the past 80 years, scientists from around the world have identified numerous mutations and genes that mediate antibiotic resistance in bacteria. The ability of antibiotics to select for bacterial mutants has revealed the degree to which mutations in bacterial genomes can alter metabolic functions and yet still support resistance expression. In addition to becoming resistant to antibiotics given systemically to patients to cure serious bacterial infections, bacterial pathogens can also demonstrate reduced susceptibility or tolerance to “multitargeting” antimicrobials such as disinfectants, antiseptics, and biocides (e.g., alcohols, essential oils, triclosan). If fact, all bacteria demonstrate a level of susceptibility to numerous antimicrobials, and certain bacterial pathogens can express “intrinsic resistance” to certain antimicrobials, which can be supported solely by their own evolved genome complement (e.g., genes encoding the outer membrane, toxin–antitoxin systems, or multidrug efflux pumps). In fact, it is now known that many intrinsic gene products are required for clinically relevant antimicrobial resistance mutations or genes to function. New knowledge on how bacteria become resistant or demonstrate reduced susceptibility to antimicrobials allows researchers to identify targets for the development of new antimicrobials.

The Section “Mechanism and Evolution of Antibiotic Resistance” seeks any and all manuscripts that describe intrinsic and horizontally transmitted genes, mutations, and mechanisms that bacteria evolve and/or utilize to remain viable during and following clinical or laboratory antimicrobial challenges. These mechanisms include the contributions of genes and mutations that support persistence, tolerance, biofilm production, and reduced susceptibility. Since we are now deep into the “omics” era, manuscripts with data from omics “fishing trips” that describe the bacterial response to antimicrobials are also sought after. Authors are also encouraged to submit molecular epidemiology projects that follow the evolution of existing antimicrobial-resistant determinants of all varieties or that contribute to our knowledge of antimicrobial resistance gene reservoirs.