Environmentally relevant concentrations of mercury facilitate the horizontal transfer of plasmid-mediated antibiotic resistance genes Original paper

What was studied?

This experimental study tested whether mercury ions (Hg²⁺) at real-world aquatic concentrations alter the rate of conjugative spread of antibiotic resistance genes (ARGs). The authors built a controlled mating system in which a donor strain carried a mobilizable plasmid (RP4) encoding resistance to multiple antibiotics, then they exposed the mixed culture to a gradient of Hg²⁺ concentrations and measured the frequency of plasmid transfer. They also measured oxidative stress and membrane injury markers and quantified expression of key plasmid-transfer regulatory genes to explain how mercury shifts the mechanics of horizontal gene transfer rather than only selecting for resistant strains after the fact.

Who was studied?

The investigators studied bacteria, not humans, using a defined donor–recipient pair to isolate the effect of mercury on gene transfer. The donor was Escherichia coli strain HB101 carrying the RP4 plasmid, and the recipient was E. coli K12 MG1655 with rifampicin resistance to enable selective counting of transconjugants. They optimized mating conditions and then conducted replicate conjugation experiments across Hg²⁺ exposures ranging from very low (0.001 mg/L) through higher levels (1.0 mg/L), while simultaneously profiling stress responses and cell structure changes that could influence contact-dependent transfer.

What were the most important findings?

Hg²⁺ at environmentally relevant concentrations (0.001–0.5 mg/L) increased plasmid-mediated ARG transfer from donor to recipient by roughly 2.4- to 5.3-fold compared with control conditions, while a higher concentration (1.0 mg/L) sharply suppressed transfer. Mechanistically, mercury exposure increased reactive oxygen species, lipid peroxidation (malondialdehyde), antioxidant enzyme activity, and membrane permeability while depleting glutathione, creating a pattern consistent with oxidative membrane injury that lowers the physical barrier to plasmid passage. Microscopy supported this mechanism by showing more apparent conjugation sites and membranes that appeared less clearly defined under Hg²⁺ exposure, which likely improved donor–recipient bridge formation at lower doses but disrupted viable mating structures at the highest dose. At the transcriptional level, Hg²⁺ reduced expression of global repressors of transfer (korA, korB, trbA) and increased expression of genes that promote mating pair formation and DNA transfer/replication (trbBp, traF, trfAp, traJ), directly aligning mercury exposure with a gene-expression program that favors conjugation.

What are the greatest implications of this study?

This work strengthens a clinically relevant One Health message: mercury pollution can actively accelerate ARG dissemination by increasing horizontal gene transfer, even when mercury levels are within ranges documented in contaminated waters. For microbiome-signature efforts, the key “signature” is functional rather than taxonomic: mercury exposure can shift bacterial physiology toward oxidative stress and membrane damage, then unlock plasmid transfer pathways that move multidrug resistance across microbes that share the same environment. Clinicians should interpret this as upstream AMR pressure that can occur outside antibiotic use, meaning resistant pathogens can emerge or intensify in aquatic systems before reaching food chains, drinking-water interfaces, or human hosts. The study also clarifies that extreme mercury levels may kill or cripple cells and reduce transfer, so risk peaks at sublethal, environmentally plausible concentrations, which reinforces the value of mercury remediation and monitoring as part of AMR prevention strategy.