Antibiotic Resistance: A Survival Strategy

Extract

Antibiotics are natural, semi-synthetic, or synthetic molecules that target the cell wall of bacteria, DNA replication, RNA transcription, or mRNA translation, the cellular machinery responsible for the synthesis of precursor molecules. Bacteria have evolved and adopted numerous strategies to counteract the action of antibiotics. Antibiotic resistance is intrinsic and an inherent characteristic of the microorganism. Intrinsic resistance is due to cell wall impermeability, efflux, biofilm formation, and the expression of genes mediating inactivating enzymes. Antibiotic resistance can also arise by the acquisition of extracellular DNA and is expressed phenotypically as efflux, modification or acquisition of target sites, and enzymatic inactivation of the antibiotic. Not only have bacteria acquired the mechanisms necessary to withstand the effects of antibiotics, they have also acquired elaborate mechanisms to mobilize and disseminate these successful strategies: plasmids, transposons, insertion sequences, and cassettes. Antibiotic resistance is a major worldwide clinical problem of public health concern because of the reduced efficacy caused by the various mechanisms of resistance. Global strategies are emerging to help address this critical problem.

Antibiotic resistance emerged soon after the discovery of antibiotics and is associated with the overuse of antimicrobial agents.¹ Although antibiotics allow the medical community to make great strides in human health and welfare, their use also causes selective pressure allowing only the fittest and less susceptible bacterial populations to survive.² Antibiotic resistance and its associated clinical failure are of such concern as to unite scientists from across the world to develop strategies to address this issue of public health concern.^3,4

ABBREVIATIONS: ABC = ATP-binding cassette; AG = aminoglycoside; CM = cytoplasmic membrane; DNA = deoxyribonucleic acid; ERM = erythromycin ribosome methylase; ESBL = extended-spectrum beta-lactamases; LPS = lipopolysaccharide; MATE = multidrug and toxic effects; MFS = major facilitator subfamily; mRNA = messenger ribonucleic acid; MRSA = methicillin-resistant Staphylococcus aureus; OM = outer membrane; PBP = penicillin-binding protein; QRDR = quinolone resistance-determining region; RNA = ribonucleic acid; RND = resistance, nodulation cell division subfamily; SMR = the small multidrug regulator; THF = tetrahydrofolate.