Genes and physiological strategies in bacterial antibiotic resistance

Bacteria display an incredible genetic plasticity, which enables them to adapt to various environmental stressors, such as antibiotic compounds that may imperil their existence. Bacterial resistance mechanisms include degradative enzymes, inactivation of antibiotics, antibacterial target site mutation, change in target, altered cell wall permeability to antibiotics, bypass of metabolic pathways, and efflux pumping of antibiotics across the cell membrane. These mechanisms are encoded by genomic changes ranging from point mutation via genetic elements assembly to horizontal transfer of genes from the environment. Antibiotic resistance in bacteria can be inherited or acquired. Antibacterial resistance genes may accumulate mobile elements, leading to multi-drug-resistant phenotypic transfer via a single genetic event. The resistance to antibiotics has been frequently increasing in clinical settings, which drives scientists to research alternative antibacterial medicines to prevent the growth and spread of drug-resistant bacteria. Technological advancements and the discovery of innovative drug moieties with targeting potential have led to the development of novel drug compounds with diverse therapeutic properties. This includes alternative cellular, physiological, and metabolic patterns of bacteria that may be potential pharmacological targets for the next generation of antibiotics. It is beneficial to characterize antibiotic resistance genotypes and phenotypes causing antibiotic bacterial resistance. An understanding of mechanisms that lead to the development and spread of antibiotic resistance will help clinicians in making appropriate decisions regarding antibiotic usage in a wide range of circumstances. The current review has highlighted the mechanism of drug resistance in bacteria, and has enlisted the antibiotic resistance genes (ARGs) and their importance in aggravating the resistance phenomenon.