Efflux pumps activation caused by mercury contamination prompts antibiotic resistance and pathogen’s virulence under ambient and elevated CO2 concentration Original paper

What was studied?

This study tested whether mercury-contaminated agricultural soil increases the abundance of plant and human pathogens and whether it strengthens antibiotic resistance and virulence by activating bacterial efflux pumps, under both current and future-like atmospheric CO₂ conditions. The researchers grew rice in clean versus legacy mercury-polluted paddy soils inside open-top chambers set to ambient CO₂ and elevated CO₂ (about +200 ppm), then used shotgun metagenomics to profile pathogen signals, efflux pump genes, and virulence factors in harvested soils.

Who was studied?

The study examined soil microbial communities associated with rice cultivation rather than human participants or animal models. The “subjects” were microbial DNA profiles from paddy soils collected from a clean field and a mercury-polluted field, incubated in replicated pots under two CO₂ environments, and sampled after a full growing period. The analysis emphasized potential plant pathogens and human pathogens detected in metagenomes and linked those taxa to functional genes tied to efflux, metal resistance, and virulence.

What were the most important findings?

Mercury contamination consistently increased the relative abundance of multiple common plant and human pathogen genera under both CO₂ conditions, with notable signals in taxa such as Xanthomonas, Pseudomonas, Salmonella, Staphylococcus, Streptococcus, Klebsiella, Mycobacterium, Magnaporthe, Dickeya, Vibrio, Yersinia, and Burkholderia. Functionally, mercury strongly increased efflux pump capacity, especially the RND family, which dominated the efflux landscape and roughly doubled in mercury soil at both CO₂ levels; the study highlighted increased abundance of key multidrug and metal efflux components including mexB, mdtA/mdtB/mdtC, acrA/acrB, and CO₂-dependent shifts that included smeD/smeF, alongside metal-linked systems such as silA and cusA/ybdE. Virulence-factor profiles shifted toward greater “offensive” potential in mercury soils, with higher representation of adherence and secretion systems and more exoenzyme-related capacity, and several adherence and secretion genes rose under both CO₂ conditions, aligning efflux activation with higher pathogenic aggressiveness. As a microbiome-signatures entry, the major association is functional: mercury selects for pathogen-enriched communities with an RND-efflux–upregulated resistome and a parallel rise in adherence/secretion-linked virulence potential.

What are the greatest implications of this study/ review?

For clinicians, this work supports a concrete bridge between environmental toxicant exposure and infection risk: mercury contamination can enrich soils for taxa that include recognized human pathogens while simultaneously selecting for mechanisms that raise antibiotic resistance potential and virulence capacity. The study also clarifies that mercury can act as a durable selection pressure that persists beyond antibiotic exposure, and that climate change context does not erase this effect, because mercury remained the dominant driver of efflux and virulence shifts under both ambient and elevated CO₂. For microbiome-informed risk assessment, the most useful signal is not a single organism but a pattern that combines pathogen enrichment with increased RND-efflux systems and virulence-associated adherence and secretion functions, suggesting that exposure history and local soil contamination can plausibly influence downstream food safety, occupational exposure risk, and the environmental reservoir that seeds resistant infections.