Antibiotic resistance is an emerging threat to human health—it renders therapeutics against pathogenic bacteria completely ineffective. Resistance emerges as an adaptive strategy for bacteria to survive in the presence of an antibiotic threat. Resistance often arises from the accumulation of random mutations that allow the microbe to survive in the presence of antibiotics. There are several mechanisms of action of mutations that cause resistance. For instance, mutations can modify the antibiotic target, modify the antibiotic itself, decrease the drug uptake by bacteria, or activate efflux mechanisms to expel the antibiotic (Munita & Arias 2016).
One of the most common mechanisms of resistance is the alteration of the drug binding site of antibiotics. Researchers have discovered that various bacteria causing urinary tract and respiratory infections, suchasEscherichia coliandStreptococcus pneumoniae, havebecome resistant to fluoroquinolone (FQ) by acquiring mutations in genes that encode the target site of FQs(LaPlante et al. 2007), which are DNA gyrase and topoisomerase IV enzymes (which are essential is bacterial DNA replication). Therefore, this resistance can be combatted by developing new antibiotics that either bind to the mutated DNA gyrase and topoisomerase IV enzymes, or that have a different lethal target.
By: Lourdes Kaufman
Munita, Jose M., and Arias, Cesar A. “Mechanisms of Antibiotic Resistance.” Microbiology Spectrum, vol. 4, no. 2, 2016, pp. Microbiology spectrum, April 2016, Vol.4(2).