Words matter. Images matter. The Scientific Inquirer needs your support. Help us pay our contributors for their hard work. Visit our Patreon page and discover ways that you can make a difference. http://bit.ly/2jjiagi
A new study’s disconcerting findings reveal how antibiotic resistance is able to spread between bacteria cells despite the presence of antibiotics that should prevent them from growing. The results reveal the ability for previously drug-sensitive bacteria to survive exposure to antibiotics long enough to express resistance genes they’ve just acquired – effectively rendering them immune to antibiotic drugs.
The mechanisms underlying this process, including a drug-jettisoning pump found in virtually all bacteria, represent targets for combatting antibiotic resistance. Bacteria can acquire new genes by receiving snippets of DNA (plasmids) from other bacteria through horizontal gene transfer mechanisms like bacterial conjugation, which often confer genetic advantages, including antibiotic resistance, in the recipient cell.
A vast array of conjugative plasmids have been identified in drug-resistant bacteria, which carry one or more resistance genes to most – if not all – clinically used antibiotic drugs. While bacterial conjugation is the primary method by which drug-resistance is spread in bacterial pathogens, many aspects of the process are poorly understood and remain to be described in vivo.
Using live-cell microscopy and a novel system for visualizing the transmission of plasmids in real time and at the cellular level, Sophie Nolivos and colleagues tracked the transfer of a plasmid carrying a tetracycline resistance gene from a drug-resistant E. coli donor bacterium to another bacterium initially susceptible to the antibiotic drug. Shortly after the plasmid-encoded genes were transferred, TetA, a protein that mediates tetracycline resistance, was rapidly produced in the recipient bacterium.
Unexpectedly, however, Nolivos et al. observed that previously antibiotic-sensitive bacteria were still able to aquire tetracycline resistance through plasmid exchange and produce the TetA resistance factor, despite being exposed to the drug. The results show that this ability stems from help from the AcrAB-TolC multidrug efflux pump of bacteria, which buys time for TetA translation by keeping tetracycline concentration below toxic levels within the bacterial cell.
IMAGE CREDIT: Creative Commons