Abstract

Discharge of treated sewage leads to release of antibiotic resistant bacteria, resistance genes and antibiotic residues to the environment. However, it is unclear whether increased abundance of antibiotic resistance genes in sewage and sewage-impacted environments is due to on-site selection pressure by residual antibiotics, or is simply a result of fecal contamination with resistant bacteria. Here we analyze relative resistance gene abundance and accompanying extent of fecal pollution in publicly available metagenomic data, using crAssphage sequences as a marker of human fecal contamination (crAssphage is a bacteriophage that is exceptionally abundant in, and specific to, human feces). We find that the presence of resistance genes can largely be explained by fecal pollution, with no clear signs of selection in the environment, with the exception of environments polluted by very high levels of antibiotics from manufacturing, where selection is evident. Our results demonstrate the necessity to take into account fecal pollution levels to avoid making erroneous assumptions regarding environmental selection of antibiotic resistance.

Highlights

  • Discharge of treated sewage leads to release of antibiotic resistant bacteria, resistance genes and antibiotic residues to the environment

  • It has been speculated that ARGs could be selected in the receiving environment by antibiotics and other coselective agents originating from the WWTP, contributing to further dissemination of ARGs to environmental bacteria[3,14,15,16]

  • We show that in practically all the studied environments, the ARG, class 1 integron (CL1), and MGE abundances correlate with fecal pollution levels with no evident signs of selection or dissemination of the resistance genes, except in sediments polluted with wastewater from drug manufacturing containing exceptionally high levels of antibiotics[33,34]

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Summary

Introduction

Discharge of treated sewage leads to release of antibiotic resistant bacteria, resistance genes and antibiotic residues to the environment. We show that in practically all the studied environments, the ARG, CL1, and MGE abundances correlate with fecal pollution levels with no evident signs of selection or dissemination of the resistance genes, except in sediments polluted with wastewater from drug manufacturing containing exceptionally high levels of antibiotics[33,34].

Results
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