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亚硝化细菌产生的亚硝酸盐介导了混合物种群落中氯胺的衰减和抗性。

Nitrite production by ammonia-oxidizing bacteria mediates chloramine decay and resistance in a mixed-species community.

机构信息

The School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW, Australia.

The Centre for Marine Bio-Innovation, The University of New South Wales, Sydney, NSW, Australia.

出版信息

Microb Biotechnol. 2020 Nov;13(6):1847-1859. doi: 10.1111/1751-7915.13628. Epub 2020 Jul 30.

DOI:10.1111/1751-7915.13628
PMID:32729670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7533321/
Abstract

As water distribution centres increasingly switch to using chloramine to disinfect drinking water, it is of paramount importance to determine the interactions of chloramine with potential biological contaminants, such as bacterial biofilms, that are found in these systems. For example, ammonia-oxidizing bacteria (AOB) are known to accelerate the decay of chloramine in drinking water systems, but it is also known that organic compounds can increase the chloramine demand. This study expanded upon our previously published model to compare the decay of chloramine in response to alginate, Pseudomonas aeruginosa, Nitrosomonas europaea and a mixed-species nitrifying culture, exploring the contributions of microbial by-products, heterotrophic bacteria and AOBs to chloramine decay. Furthermore, the contribution of AOBs to biofilm stability during chloramination was investigated. The results demonstrate that the biofilm matrix or extracellular polymeric substances (EPS), represented by alginate in these experiments, as well as high concentrations of dead or inactive cells, can drive chloramine decay rather than any specific biochemical activity of P. aeruginosa cells. Alginate was shown to reduce chloramine concentrations in a dose-dependent manner at an average rate of 0.003 mg l  h per mg l of alginate. Additionally, metabolically active AOBs mediated the decay of chloramine, which protected members of mixed-species biofilms from chloramine-mediated disinfection. Under these conditions, nitrite produced by AOBs directly reacted with chloramine to drive its decay. In contrast, biofilms of mixed-species communities that were dominated by heterotrophic bacteria due to either the absence of ammonia, or the addition of nitrification inhibitors and glucose, were highly sensitive to chloramine. These results suggest that mixed-species biofilms are protected by a combination of biofilm matrix-mediated inactivation of chloramine as well as the conversion of ammonia to nitrite through the activity of AOBs present in the community.

摘要

随着越来越多的水分配中心开始使用氯胺来消毒饮用水,确定氯胺与系统中发现的潜在生物污染物(如细菌生物膜)的相互作用至关重要。例如,氨氧化细菌(AOB)已知会加速饮用水系统中氯胺的衰减,但也知道有机化合物会增加氯胺的需求。本研究扩展了我们之前发表的模型,以比较在响应藻酸盐、铜绿假单胞菌、欧洲亚硝化单胞菌和混合硝化培养物时氯胺的衰减,探索微生物副产物、异养细菌和 AOB 对氯胺衰减的贡献。此外,还研究了 AOB 对氯胺消毒过程中生物膜稳定性的贡献。结果表明,生物膜基质或细胞外聚合物物质(EPS),在这些实验中由藻酸盐代表,以及高浓度的死细胞或无活性细胞,可驱动氯胺衰减,而不是铜绿假单胞菌细胞的任何特定生化活性。藻酸盐表现出以剂量依赖的方式降低氯胺浓度,平均速率为每毫克藻酸盐 0.003 毫克/升/小时。此外,代谢活跃的 AOB 介导了氯胺的衰减,从而保护了混合物种生物膜免受氯胺介导的消毒。在这些条件下,AOB 产生的亚硝酸盐直接与氯胺反应,驱动其衰减。相比之下,由于缺乏氨或添加硝化抑制剂和葡萄糖,混合物种生物膜中的异养细菌占主导地位,对氯胺非常敏感。这些结果表明,混合物种生物膜受到生物膜基质介导的氯胺失活以及通过存在于群落中的 AOB 将氨转化为亚硝酸盐的组合的保护。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/50bd4fdeb467/MBT2-13-1847-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/2ded78e7b59b/MBT2-13-1847-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/d2d49fa987fd/MBT2-13-1847-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/789e67504bb5/MBT2-13-1847-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/b634c06cc424/MBT2-13-1847-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/d0340a80aba7/MBT2-13-1847-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/50bd4fdeb467/MBT2-13-1847-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/2ded78e7b59b/MBT2-13-1847-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/d2d49fa987fd/MBT2-13-1847-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/789e67504bb5/MBT2-13-1847-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/b634c06cc424/MBT2-13-1847-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/d0340a80aba7/MBT2-13-1847-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c6/7533321/50bd4fdeb467/MBT2-13-1847-g006.jpg

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