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基因组可塑性作为ESKAPE病原体中抗生素耐药性传播的范例。

Genome plasticity as a paradigm of antibiotic resistance spread in ESKAPE pathogens.

作者信息

Das Sanchita, Bombaywala Sakina, Srivastava Shweta, Kapley Atya, Dhodapkar Rita, Dafale Nishant A

机构信息

Environmental Biotechnology and Genomics Division, CSIR-National Environmental Engineering Research Institute (CSIR-NEERI), Nehru Marg, Nagpur, 4400 20, India.

Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 2010 20, India.

出版信息

Environ Sci Pollut Res Int. 2022 Jun;29(27):40507-40519. doi: 10.1007/s11356-022-19840-5. Epub 2022 Mar 29.

DOI:10.1007/s11356-022-19840-5
PMID:35349073
Abstract

The major reason behind the spread of antibiotic resistance genes (ARGs) is persistent selective pressure in the environment encountered by bacteria. Genome plasticity plays a crucial role in dissemination of antibiotic resistance among bacterial pathogens. Mobile genetic elements harboring ARGs are reported to dodge bacterial immune system and mediate horizontal gene transfer (HGT) under selective pressure. Residual antibiotic pollutants develop selective pressures that force the bacteria to lose their defense mechanisms (CRISPR-cas) and acquire resistance. The present study targets the ESKAPE organisms (namely, Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter spp.) causing various nosocomial infections and emerging multidrug-resistant species. The role of CRISPR-cas systems in inhibition of HGT in prokaryotes and its loss due to presence of various stressors in the environment is also focused in the study. IncF and IncH plasmids were identified in all strains of E. faecalis and K. pneumoniae, carrying Beta-lactam and fluoroquinolone resistance genes, whereas sal3, phiCTX, and SEN34 prophages harbored aminoglycoside resistance genes (aadA, aac). Various MGEs present in selected environmental niches that aid the bacterial genome plasticity and transfer of ARGs contributing to its spread are also identified.

摘要

抗生素耐药基因(ARGs)传播的主要原因是细菌在环境中面临的持续选择性压力。基因组可塑性在细菌病原体之间抗生素耐药性的传播中起着关键作用。据报道,携带ARGs的移动遗传元件能够躲避细菌免疫系统,并在选择性压力下介导水平基因转移(HGT)。残留的抗生素污染物产生选择性压力,迫使细菌失去其防御机制(CRISPR-cas)并获得耐药性。本研究针对引起各种医院感染和新出现的多重耐药菌的ESKAPE病原体(即粪肠球菌、金黄色葡萄球菌、肺炎克雷伯菌、鲍曼不动杆菌、铜绿假单胞菌和肠杆菌属)。该研究还聚焦了CRISPR-cas系统在原核生物中抑制HGT的作用以及由于环境中各种应激源的存在导致其丧失的情况。在所有粪肠球菌和肺炎克雷伯菌菌株中均鉴定出携带β-内酰胺和氟喹诺酮耐药基因的IncF和IncH质粒,而sal3、phiCTX和SEN34前噬菌体则携带氨基糖苷类耐药基因(aadA、aac)。还确定了存在于选定环境生态位中的各种移动遗传元件,这些元件有助于细菌基因组可塑性和ARGs的转移,从而导致其传播。

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