Tetracycline and Chloramphenicol Resistance Mechanisms

Abstract

Tetracycline resistance (Tcr) is most often due to the acquisition of new genes, which code for energy-dependent effl ux of tetracyclines, or for a protein that protects bacterial ribosomes from the action of tetracyclines. Many of these genes are associated with mobile plasmids or transposons and can be distinguished from each other using molecular methods including DNA-DNA hybridization with oligonucleotide probes and DNA sequencing. A limited number of bacteria acquire Tcr by mutations, which alter the permeability of the outer membrane porins and/or lipopolysaccharides in the outer membrane, change regulation of innate effl ux systems, or alter the 16S rRNA (1). Currently, two genes are considered related, i.e., of the same class, and given the same gene designation if their gene products share 80{%} of the amino acid sequences in common with each other. Two genes are considered different from each other if their gene products share 79{%} amino acid sequence identity (2). This comparison can now be done using the GenBank sequence information.