> "Furthermore, no mutations were observed that affect any of the numerous efflux pumps, which were readily obtained using the same approach for ciprofloxacin resistance, suggesting that COE2-2hexyl is not an efflux pump substrate or effector. MDR [Multi-drug-resistant] pathogens whose resistance is driven primarily by pre-existing efflux upregulation would thus remain susceptible to COEs."
The ability of infectious microbes to rapidly pump antibiotics out of their cells is a main feature of the rise of antibiotic resistance, and is a core element of microbial physiology:
"Bacterial Multidrug Efflux Pumps: Much More Than Antibiotic Resistance Determinants" (2016)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029519/
So, they're saying they see no evidence that this class of compounds is targeted by any known efflux pump protein complexes, and thus resistance by that route is unlikely to quickly develop. This however doesn't rule out other mechanisms, such as the infectious bacteria acquiring enzyme genes that allow it to cleave the molecule, etc.
As far as selective pressure, one main culprit in the rise of antibiotic resistance was their use in industrial farming systems, in which animals confined side by side are given steady doses of antibiotics as a preventive measure and for growth-promotion, which results in a steady evolutionary selective pressure for mutations that conferred resistance. Widespread prescription by doctors to human patients who might have just had viral infections, and lack of enforcement of the full course of antibiotics also were at fault, but factory farming practices seem to be the main issue (note the EU banned much of this in 2006):
> "Animals on U.S. factory farms consume over 80 percent of the nation’s antibiotics; a nine percent rise in the sale of antibiotics used in U.S. animal feed between 2017 and 2018 indicates that antibiotic usage by factory farms is still increasing."
https://sentientmedia.org/the-indisputable-link-between-anti...