Class 1 integrons in clinical isolates of Staphylococcus aureus and its relation to antibiotic resistance

The bactericidal effect of beta-lactams is linked to the inhibition of transpeptidation, by binding to PLPs, generating deficient areas in the bacterial wall, allowing the passage of substances from the medium into the interior of the microorganisms, causing death by osmotic shock. Bacterial Acquired resistance is based on genetics and can derive from a chromosomal mutation or through the acquisition of transferable (extrachromosomal) genetic material. Resistance coding genes can be located both on the bacterial chromosome and outside of it, in plasmids, transposons and integrons, the latter also chromosomally located. The main cause of resistance to beta-lactams, both in Gram-positive and Gram-negative bacteria, is the production of beta-lactamases. These enzymes have the ability to hydrolyze the amide bond of the beta-lactam ring, a common element within the structure of penicillins, cephalosporins, cephamycins and carbapenems, giving rise to a compound without antibacterial activity. The appearance and dissemination of MRSA is favored by the lack of hygienic measures to prevent the spread of microorganisms in hospitals, and by the selective pressure that the high consumption of antibiotics in these centers entails.