摘要

抗生素耐药性的出现和传播对人类健康和环境生态系统构成了重大威胁。虽然消毒已被证明有效控制病原体的发生，但很少有努力致力于揭示消毒对抗生素抗性基因（ARG）传播的潜在影响，特别是对于城市废水处理的最终消毒废水中的自由生活ARGs植物（UWWTP）。在这里，我们调查了一年中氯消毒对细胞外ARGs（eARGs）和细胞内ARGs（iARGs）在全尺寸UWWTP中的发生和浓度的影响。我们报道了用二氧化氯（ClO2）消毒可以增加eARGs和iARGs的浓度。具体而言，氯化优先增加eARG对大环内酯（ermB），四环素（tetA，tetB和tetC），磺胺（sul1，sul2和sul3），β-内酰胺（ampC），氨基糖苷类（aph（2'） - ，利福平（katG）和万古霉素（vanA）高达3.8倍。同样，氯化后iARG的丰度也增加了7.8倍。在相关分析中，氯化前大肠杆菌的丰度与总eARG浓度呈显着正相关，而低温和高铵浓度则与iARG浓度呈正相关。这项研究表明氯消毒可以增加iARGs和eARGs的丰度，从而导致在环境中传播抗生素耐药性的风险。

The emergence and spread of antibiotic resistance has posed a major threat to both human health and environmental ecosystem. Although the disinfection has been proved to be efficient to control the occurrence of pathogens, little effort is dedicated to revealing potential impacts of disinfection on transmission of antibiotic resistance genes (ARGs), particularly for free-living ARGs in final disinfected effluent of urban wastewater treatment plants (UWWTP). Here, we investigated the effects of chlorine disinfection on the occurrence and concentration of both extracellular ARGs (eARGs) and intracellular ARGs (iARGs) in a full-scale UWWTP over a year. We reported that the concentrations of both eARGs and iARGs would be increased by the disinfection with chlorine dioxide (ClO2). Specifically, chlorination preferentially increased the abundances of eARGs against macrolide (ermB), tetracycline (tetA, tetB and tetC), sulfonamide (sul1, sul2 and sul3), β-lactam (ampC), aminoglycosides (aph(2’)-Id), rifampicin (katG) and vancomycin (vanA) up to 3.8 folds. Similarly, the abundances of iARGs were also increased up to 7.8 folds after chlorination. In terms of correlation analyses, the abundance of Escherichia coli before chlorination showed a strong positive correlation with the total eARG concentration, while lower temperature and higher ammonium concentration were assumed to be associated with the concentration of iARGs. This study suggests the chlorine disinfection could increase the abundances of both iARGs and eARGs, thereby posing risk of the dissemination of antibiotic resistance in environments.

https://www.sciencedirect.com/science/article/pii/S004313541830143X