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Emergence of colistin resistance in multidrug-resistant Klebsiella pneumoniae and Escherichia coli strains isolated from cancer patients
Annals of Clinical Microbiology and Antimicrobials ( IF 4.6 ) Pub Date : 2019-12-12 , DOI: 10.1186/s12941-019-0339-4
Mai M Zafer 1 , Hadir A El-Mahallawy 2 , Asmaa Abdulhak 1 , Magdy A Amin 3 , Mohamed H Al-Agamy 4, 5 , Hesham H Radwan 4
Affiliation  

Colistin resistance is mainly driven by alterations in the Gram-negative outer membrane lipopolysaccharides and is caused, in most cases, by mutations in mgrB gene. However, the recent emergence of plasmid-encoded colistin resistance among Enterobacteriaceae strains represents a serious threat to global public health. In this paper we have investigated the rates of colistin resistance and the underlying mechanisms in 450 Klebsiella pneumoniae and Escherichia coli isolates obtained from cancer patients in Egypt. Colistin susceptibility and minimum inhibitory concentrations were determined according to the European Committee on Antimicrobial Susceptibility Testing, by broth microdilution, and by E-test. The mcr-1, mcr-2 and mgrB genes were detected by PCR and then sequenced. Clonal diversity in colistin-resistant K. pneumoniae was evaluated by multilocus sequence typing. Forty (8.8%) colistin-resistant isolates, including 22 K. pneumoniae and 18 E. coli, were isolated over 18 months. Of these, 50% were carbapenem-resistant, out of which nine were blaOXA-48 and seven blaNDM-1 positive. The mechanisms of colistin resistance could be revealed only in three of the 40 resistant strains, being represented by mcr-1 in one blaNDM-1-positive E. coli strain and in one K. pneumoniae ST11 and by mgrB mutations, detected in one K. pneumoniae isolate. None of the studied isolates harbored mcr-2. Our results demonstrate a high frequency of colistin resistance in enterobacterial strains isolated from cancer patients, but a low prevalence of the most well known resistance mechanisms.

中文翻译:

分离自癌症患者的耐多药肺炎克雷伯菌大肠埃希菌菌株中大肠菌素耐药性的出现

共利斯汀抗性主要是由革兰氏阴性外膜脂多糖的变化驱动的,并且在大多数情况下是由mgrB基因突变引起的。但是,最近在肠杆菌科菌株中出现质粒编码的大肠菌素抗性,这对全球公共卫生构成了严重威胁。在本文中,我们研究了从埃及癌症患者获得的450株肺炎克雷伯菌和大肠杆菌分离株中大肠菌素耐药率及其潜在机制。根据欧洲抗菌药物敏感性试验委员会,肉汤微量稀释法和E检验,确定了共利斯汀的药敏度和最低抑菌浓度。通过PCR检测mcr-1,mcr-2和mgrB基因,然后测序。大肠菌素抗性K的克隆多样性 通过多基因座序列分型评估肺炎。在18个月内分离出了40种(8.8%)抵抗大肠菌素的菌株,包括22株肺炎克雷伯菌和18株大肠杆菌。其中,有50%对碳青霉烯有抗药性,其中9种为blaOXA-48和7种blaNDM-1阳性。仅在40株耐药菌株中的3株中揭示了大肠菌素耐药性的机制,以一株blaNDM-1阳性大肠杆菌菌株中的mcr-1和一株肺炎克雷伯菌ST11为代表,并在一个K中检测到mgrB突变。肺炎分离株 所研究的分离株均未携带mcr-2。我们的结果表明,从癌症患者分离出的肠杆菌菌株中大肠菌素耐药性的发生频率很高,但最广为人知的耐药机制的发生率较低。在18个月内分离出肺炎链球菌和18株大肠杆菌。其中,有50%对碳青霉烯有抗药性,其中9种为blaOXA-48和7种blaNDM-1阳性。仅在40株耐药菌株中的3株中揭示了大肠菌素耐药性的机制,以一株blaNDM-1阳性大肠杆菌菌株中的mcr-1和一株肺炎克雷伯菌ST11为代表,并在一个K中检测到mgrB突变。肺炎分离株 所研究的分离株均未携带mcr-2。我们的结果表明,从癌症患者分离出的肠杆菌菌株中大肠菌素耐药性的发生频率很高,但最广为人知的耐药机制的发生率较低。在18个月内分离出肺炎链球菌和18株大肠杆菌。其中,有50%对碳青霉烯有抗药性,其中9种为blaOXA-48和7种blaNDM-1阳性。仅在40株耐药菌株中的3株中揭示了大肠菌素耐药性的机制,以一株blaNDM-1阳性大肠杆菌菌株中的mcr-1和一株肺炎克雷伯菌ST11为代表,并在一个K中检测到mgrB突变。肺炎分离株 所研究的分离株均未携带mcr-2。我们的结果表明,从癌症患者分离出的肠杆菌菌株中大肠菌素耐药性的发生频率很高,但最广为人知的耐药机制的发生率较低。仅在40株耐药菌株中的3株中揭示了大肠菌素耐药性的机制,以一株blaNDM-1阳性大肠杆菌菌株中的mcr-1和一株肺炎克雷伯菌ST11为代表,并在一个K中检测到mgrB突变。肺炎分离株 所研究的分离株均未携带mcr-2。我们的结果表明,从癌症患者分离出的肠杆菌菌株中大肠菌素耐药性的发生频率很高,但最广为人知的耐药机制的发生率较低。仅在40株耐药菌株中的3株中揭示了大肠菌素耐药性的机制,以一株blaNDM-1阳性大肠杆菌菌株中的mcr-1和一株肺炎克雷伯菌ST11为代表,并在一个K中检测到mgrB突变。肺炎分离株 所研究的分离株均未携带mcr-2。我们的结果表明,从癌症患者分离出的肠杆菌菌株中大肠菌素耐药性的发生频率很高,但最广为人知的耐药机制的发生率较低。
更新日期:2020-04-22
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