摘要

含有抗生素和高盐度的制药废水可能会损害传统的生物处理并导致抗生素抗性基因（ARG）的增殖。生物电化学系统（BES）是一种很有前景的处理制药废水的方法。然而，BES中的ARGs的命运及其与微生物群落和水平基因转移的相关性是未知的。在这项研究中，我们研究了ARGs对不同盐度下氯霉素废水及其潜在宿主的生物电化学处理的响应。分析编码外排泵（cmlA，floR和tetC），一个1类整合子整合酶编码基因（intI1）和sul1基因（与intI1相关）的三个ARGs。微生物群落与ARGs的相关分析表明，ARGs潜在寄主的丰度受盐度的强烈影响，这进一步决定了不同盐度下ARGs丰度的变化。 ARGs与intI1之间没有显着相关性，表明水平基因转移与ARGs的重要变化无关。此外，由于受盐度驱动的微生物群落改变，在适度的盐度下氯霉素去除效率增强。因此，微生物群落转换是不同盐度下BES中ARGs和氯霉素去除效率变化的主要因素。本研究为BES处理高盐制药废水中ARGs改变的机制提供了新的见解。

Pharmaceutical wastewaters containing antibiotics and high salinity can damage traditional biological treatment and result in the proliferation of antibiotic resistance genes (ARGs). Bioelectrochemical system (BES) is a promising approach for treating pharmaceutical wastewater. However, the fate of ARGs in BES and their correlations with microbial communities and horizontal genes transfer are unknown. In this study, we investigated the response of ARGs to bio-electrochemical treatment of chloramphenicol wastewater and their potential hosts under different salinities. Three ARGs encoding efflux pump (cmlA, floRand tetC), one class 1 integron integrase encoding gene (intI1), and sul1 gene (associate with intI1) were analyzed. Correlation analysis between microbial community and ARGs revealed that the abundances of potential hosts of ARGs were strongly affected by salinity, which further determined the alteration in ARGs abundances under different salinities. There were no significant correlations between ARGs and intI1, indicating that horizontal gene transfer was not related to the important changes in ARGs. Moreover, the chloramphenicol removal efficiency was enhanced under a moderate salinity, attributed to the altered microbial community driven by salinity. Therefore, microbial community shift is the major factor for the changes of ARGs and chloramphenicol removal efficiency in BES under different salinities. This study provides new insights on the mechanisms underlying the alteration of ARGs in BES treating high-salinity pharmaceutical wastewater.

https://www.sciencedirect.com/science/article/pii/S0043135418300241