摘要

       抗生素在环境中的广泛传播，对微生物的耐药性产生了巨大的压力。海洋微生物群是新抗生素和相应耐药基因的大库。坎巴特湾以其极端的潮汐和复杂的沉积过程而闻名。我们通过高通量测序和应用生物信息学技术对Khambhat湾四个坐标的远洋沉积物微生物群进行了评估，评估了海洋抗性及其相应的细菌群落，并与开放的阿拉伯海样本进行了比较。我们共鉴定了2354种独特类型的抗病基因，其中最丰富和多样的基因图谱是在岸上进行人类活动的地区。所有样本中丰度大于1%的基因包括carA、macB、sav1866、tlrC、srmB、taeA、tetA、oleC和bcrA，它们属于大环内酯类、糖肽类和肽类药物。富含精氨酸的门在各部位的分布差异很大，其中以蛋白菌、厚壁菌、放线菌和拟杆菌为主。基于这些结果，我们还提出了潜在的生物标记物候选脱硫弧菌、热菌和嗜酸杆菌，用于监测两个海湾样品中可能存在污染的环境中的抗生素，以及其余三个研究样品中的亚硝基球菌属、马里诺杆菌属和链霉菌属。结果支持ARGs自然起源于环境和人类活动有助于传播抗生素耐药性的概念。

        Antibiotics have been widely spread in the environments, imposing profound stress on the resistome of the residing microbes. Marine microbiomes are well established large reservoirs of novel antibiotics and corresponding resistance genes. The Gulf of Khambhat is known for its extreme tides and complex sedimentation process. We performed high throughput sequencing and applied bioinformatics techniques on pelagic sediment microbiome across four coordinates of the Gulf of Khambhat to assess the marine resistome, its corresponding bacterial community and compared with the open Arabian Sea sample. We identified a total of 2354 unique types of resistance genes, with most abundant and diverse gene profile in the area that had anthropogenic activities being carried out on-shore. The genes with >1% abundance in all samples included carA, macB, sav1866, tlrC, srmB, taeA, tetA, oleC and bcrA which belonged to the macrolides, glycopeptides and peptide drug classes. ARG enriched phyla distribution was quite varying between all the sites, with Proteobacteria, Firmicutes, Actinobacteria and Bacteroidetes among the dominant phyla. Based on the outcomes, we also propose potential biomarker candidates Desulfovibrio, Thermotaga and Pelobacter for antibiotic monitoring in the two of the Gulf samples probable contamination prone environments, and genera Nitrosocccus, Marinobacter and Streptomyces in the rest of the three studied samples. Outcomes support the concept that ARGs naturally originate in environments and human activities contribute to the dissemination of antibiotic resistance.

        https://www.sciencedirect.com/science/article/pii/S0048969718343092?via%3Dihub