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Pyraclostrobin and polyethylene nanoplastics jointly interfere with the antibiotic resistome in earthworm gut

Biology and Fertility of Soils 2025 5 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
H. J. Yang, Conglai Zheng, Enbo Zhang, Guy Smagghe, Shun‐Hua Gui, Xiaomao Wu, Xiaomao Wu, Xiangsheng Chen, Xiangsheng Chen

Summary

Researchers exposed earthworms to polyethylene nanoplastics and the fungicide pyraclostrobin, finding that the combination increased antibiotic resistance gene diversity and abundance in earthworm guts, expanded the range of bacterial hosts carrying resistance genes, and elevated mobile genetic elements — suggesting nanoplastics may accelerate the spread of antibiotic resistance through soil ecosystems.

Antibiotic resistance has emerged as a global threat to public health. However, the current information is insufficient to understand how other pollutants, such as fungicides and nanoplastics, affect the spread of antibiotic resistance genes (ARGs) among bacteria in the soil. Here, our findings revealed that polyethylene nanoplastics (PENPs) prolonged the persistence of pyraclostrobin (PYR) in the soil by 13 days, increased PYR bioaccumulation in earthworm (Eisenia fetida) by 8.4%, and reduced its weights by 26.8%. PYR alone or combined with PENPs significantly increased the microbiome diversities of earthworm guts, while PENPs alone decreased those but increased the relative abundances of Proteobacteria and Firmicute. PYR and/or PENPs enhanced the diversity and abundance of ARGs in earthworm guts, the range of ARG hosts, and the complexity of ARGs and antibiotic-resistant bacteria coexistence network. The abundance of plasmid-origin ARG-harboring contigs in PYR, PENP, and PYR + PENP treatments was 1.5-, 3.8-, and 2.4-fold higher than that in the control, respectively. Overall, PYR and/or PENPs specifically disturbed the antibiotic resistome in earthworm guts by altering the bacterial community composition and richness, increasing the abundance of mobile genetic elements (MGEs) and ARGs, and modifying the co-occurrence pattern of ARGs-MGEs, particularly plasmids.

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