Department of Medical Microbiology, Pathology Building, University of Pretoria, Prinshof Campus, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa; Tshwane Academic Division, National Health Laboratory Service, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa.
Department of Medical Microbiology, Pathology Building, University of Pretoria, Prinshof Campus, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa; Tshwane Academic Division, National Health Laboratory Service, Corner of Steve Biko Road and Dr Savage Road, Pretoria 0084, South Africa.
J Glob Antimicrob Resist. 2019 Dec;19:164-166. doi: 10.1016/j.jgar.2019.09.014. Epub 2019 Sep 23.
The underlying resistance mechanism and phylogenetic relationship of a colistin-resistant Salmonella enterica serovar Enteritidis strain EC20120916 that resulted in fatal meningitis in an immunocompromised patient was investigated by whole-genome sequencing (WGS) analysis.
WGS of strain EC20120916 was performed on an Illumina MiSeq platform and annotation of the sequence was performed using the Prokaryotic Genome Annotation Pipeline (PGAP). Antimicrobial resistance genes, plasmid replicons and pathogenicity islands were identified. A phylogenetic tree was constructed using Parsnp and was edited with FigTree.
The genome size of strain EC20120916 is 4 699 318 bp with a GC content of 55.2% and 4471 protein-coding genes. The aac(6')-laa gene, encoding resistance to aminoglycosides, was identified although this was not expressed phenotypically in the isolate. No colistin resistance-conferring mutations or plasmid-mediated mechanisms were identified to explain the colistin resistance. The strain was phylogenetically related to three international strains, although it was not close enough to suggest importation from outside of South Africa.
This is the first report of a colistin-resistant Salmonella Enteritidis isolate causing meningitis in an immunocompromised patient in South Africa. The absence of colistin resistance-conferring mutations or plasmid-mediated resistance mechanisms suggest that a novel mechanism is responsible for the colistin resistance in this isolate. The isolate was acquired locally.
通过全基因组测序（WGS）分析，研究导致免疫功能低下患者致命性脑膜炎的耐粘菌素肠炎沙门氏菌血清型肠炎亚种 EC20120916 菌株的潜在耐药机制和系统发育关系。
在 Illumina MiSeq 平台上对 EC20120916 菌株进行 WGS，使用 Prokaryotic Genome Annotation Pipeline（PGAP）对序列进行注释。鉴定了抗生素耐药基因、质粒复制子和致病性岛。使用 Parsnp 构建系统发育树，并使用 FigTree 编辑。
EC20120916 菌株的基因组大小为 4699318 bp，GC 含量为 55.2%，有 4471 个编码蛋白的基因。尽管该分离株在表型上没有表达，但鉴定出了编码对氨基糖苷类药物耐药的 aac(6')-laa 基因。没有发现与粘菌素耐药相关的突变或质粒介导的机制来解释粘菌素耐药。该菌株与三个国际菌株在系统发育上有关，但与提示从南非境外输入的菌株还不够接近。
这是南非首例耐粘菌素肠炎沙门氏菌肠炎亚种分离株引起免疫功能低下患者脑膜炎的报告。缺乏粘菌素耐药相关突变或质粒介导的耐药机制表明，该分离株的粘菌素耐药是由一种新的机制引起的。该分离株是在当地获得的。
