Draft genome sequence of blaTEM-1-mediated cephalosporin-resistant Salmonella enterica serovar Typhi from bloodstream infection

被引:18
作者
Ragupathi, Naveen Kumar Devanga [1 ]
Sethuvel, Dhiviya Prabaa Muthuirulandi [1 ]
Shankar, Baby Abirami [1 ]
Munusamy, Elakkiya [1 ]
Anandan, Shalini [1 ]
Veeraraghavan, Balaji [1 ]
机构
[1] Christian Med Coll & Hosp, Dept Clin Microbiol, Vellore 632004, Tamil Nadu, India
关键词
Salmonella Typhi; Cephalosporin resistance; bla(TEM); IncN plasmid; Bloodstream infection; qnr; GENES;
D O I
10.1016/j.jgar.2016.06.003
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Enteric fever is a major cause of concern in developing countries across the globe. The primary choice of antibiotics remains fluoroquinolones, followed by cephalosporins. Resistance to third-generation cephalosporins is rarely reported in Salmonella enterica serovar Typhi. This study reports the whole genome sequence of an S. Typhi isolate resistant to cefixime [minimum inhibitory concentration (MIC) = 512 mu g/mL] by microbroth dilution. Interestingly, the isolate was negative for the cephalosporin resistance gene bla(CTX-M) by PCR, which is a known mechanism for higher cephalosporin resistance. The isolate was further subjected to next-generation sequencing that identified bla(TEM-1B) and bla(DHA-1) genes in association with qnrB4 and sul1. bla(TEM) is a known gene coding for beta-lactam resistance. In certain cases, overexpression of bIaTEM was reported to result in cephalosporin resistance. This suggests that the high cefixime MIC would have been contributed by overexpression of bla(TEM-1B). The bla(TEM-1B) gene was found to be associated with a promoter Px with -35 and -10 regions as TTAATA and TAAAGT, respectively. The promoter regions were unique, but the -10 region was similar to that found in Pa/Pb (previously reported promoter for bIaTEM) with a single nucleotide change. In addition, an IncN plasmid was identified, which is usually reported in association with the most prevalent extended-spectrum beta-lactamase (ESBL), metallo-and non-metallo-carbapenemase, and plasmid-mediated quinolone resistance (PMQR) genes. Plasmids such as IncN might possibly confer resistance and enhance spread. It is imperative to continuously monitor the drug resistance profile and evolving genetic elements. (C) 2016 International Society for Chemotherapy of Infection and Cancer. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:11 / 12
页数:2
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