期刊
MICROBIAL DRUG RESISTANCE
卷 27, 期 10, 页码 1405-1411出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/mdr.2020.0395
关键词
whole-genome sequencing; pandrug resistance; Klebsiella pneumoniae; AcrAB-TolC; acrR; ramR
资金
- Natural Science Foundation of Guangdong Province [2015A030313522]
- Science and Technology Plan projects (field of Social Development) of Guangdong province [2016A020215150]
- 2019 Dongguan social science and technology development (key) project [201950715046197]
- Open projects of R&D public service platform of South China Sea marine medicine resource of Guangdong Medical University [201819]
KPN142, a clinically isolated pan-resistant strain of Klebsiella pneumoniae, showed limited antibiotic resistances mediated mainly by enzymes, with efflux pumps contributing most to pan resistance. Overexpression of the AcrAB-TolC efflux pump system played a key role in the resistance pattern of KPN142, while absence of suppressor gene mgrB and overexpression of phoPQ contributed to its resistance to colistin B.
A clinically isolated pan-resistant Klebsiella pneumoniae strain (ST11), KPN142 was subjected to whole-genome sequencing. Genomic sequence of KPN142 showed that limited antibiotic resistances (beta-lactams [bla(shv-11)], sulfonamides [sul1 and dfrA22], bacitracin [bacA], tetracycline [tet34], aminoglycosides [ksgA, kdpE, aph(3)Ia, aac(3)III, and ant(3)Ia], and chloramphenicol [catA1]) were mediated by enzymes, and efflux pumps contributed most to pan resistance. Five types of multidrug resistance efflux pump families were identified, including the resistance nodulation division superfamily (AcrAB-TolC, AcrD, MdtABC, and KexD), the ATP-binding cascade superfamily (MacAB), the small multidrug resistance family (KpnEF), the multidrug and toxic compound extrusion family (KdeA), and the major facilitator superfamily (EmrAB). There was an AcrAB-TolC efflux pump system, and inhibitory regulatory gene acrR and ramR of system carried deletion mutation, which lead to overexpression of AcrAB-TolC efflux pump, and in turn plays key role in the pan resistance of KPN142. Moreover, we did not find mgrb, a suppressor in the expression of phoPQ, overexpression of which may confer the resistance of KPN142 to colistin B. In addition, K. pneumoniae KPN142 carries IS1, IS3, and IntI1, which means that KPN142 is able to transfer drug-resistance genes. Of note, we detected the overexpression of acrB, ramA, phoP, and phoQ by real-time quantitative reverse transcription-polymerase chain reaction, and carbonyl cyanide chlorophenylhydrazone was able to reverse the resistance patterns of K. pneumoniae KPN142. In conclusion, we consider that the overexpression of AcrAB-TolC efflux pump mediates the resistance to most common clinical antimicrobial agents, and the overexpression of phoPQ mediates the resistance to colistin B in K. pneumoniae KPN142.
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