Subinhibitory Concentrations of Disinfectants Promote the Horizontal Transfer of Multidrug Resistance Genes within and across Genera

氯胺 消毒剂 大肠杆菌 微生物学 过氧化氢 膜透性 抗生素耐药性 多重耐药 生物 细菌 抗生素 基因 水平基因转移 化学 生物化学 遗传学 系统发育学 有机化学
作者
Ye Zhang,April Z. Gu,Miao He,Dan Li,Jianmin Chen
出处
期刊:Environmental Science & Technology [American Chemical Society]
卷期号:51 (1): 570-580 被引量:419
标识
DOI:10.1021/acs.est.6b03132
摘要

The greater abundances of antibiotic resistance genes (ARGs) in point-of-use tap and reclaimed water than that in freshly treated water raise the question whether residual disinfectants in distribution systems facilitate the spread of ARGs. This study investigated three widely used disinfectants (free chlorine, chloramine, and hydrogen peroxide) on promoting ARGs transfer within Escherichia coli strains and across genera from Escherichia coli to Salmonella typhimurium. The results demonstrated that subinhibitory concentrations (lower than minimum inhibitory concentrations [MICs]) of these disinfectants, namely 0.1–1 mg/L Cl2 for free chlorine, 0.1–1 mg/L Cl2 for chloramine, and 0.24–3 mg/L H2O2, led to concentration-dependent increases in intragenera conjugative transfer by 3.4–6.4, 1.9–7.5, and 1.4–5.4 folds compared with controls, respectively. By comparison, the intergenera conjugative frequencies were slightly increased by approximately 1.4–2.3 folds compared with controls. However, exposure to disinfectants concentrations higher than MICs significantly suppressed conjugative transfer. This study provided evidence and insights into possible underlying mechanisms for enhanced conjugative transfer, which involved intracellular reactive oxygen species formation, SOS response, increased cell membrane permeability, and altered expressions of conjugation-relevant genes. The results suggest that certain oxidative chemicals, such as disinfectants, accelerate ARGs transfer and therefore justify motivations in evaluating disinfection alternatives for controlling antibiotic resistance. This study also triggers questions regarding the potential role of environmental chemicals in the global spread of antibiotic resistance.
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