| Literature DB >> 31315959 |
Xuebing Wang1, Haijian Zhou1, Dongke Chen2, Pengcheng Du3, Ruiting Lan4, Xiaotong Qiu1, Xuexin Hou1, Zhiguo Liu1, Lina Sun1, Shuai Xu1, Xingzhao Ji1, Heqiao Li5, Dan Li1, Jingshan Zhang1, Hui Zeng3, Zhenjun Li6.
Abstract
Corynebacterium striatum is an emerging multidrug-resistant (MDR) pathogen that occurs primarily among immunocompromised and chronically ill patients. However, little is known about the genomic diversity of C. striatum, which contributes to its long-term persistence and transmission in hospitals. In this study, a total of 192 C. striatum isolates obtained from 14 September 2017 to 29 March 2018 in a hospital in Beijing, China, were analyzed by antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE). Whole-genome sequencing was conducted on 91 isolates. Nearly all isolates (96.3%, 183/190) were MDR. The highest resistance rate was observed for ciprofloxacin (99.0%, 190/192), followed by cefotaxime (90.6%, 174/192) and erythromycin (89.1%, 171/192). PFGE separated the 192 isolates into 79 pulsotypes, and differences in core genome single-nucleotide polymorphisms (SNPs) partitioned the 91 isolates sequenced into four clades. Isolates of the same pulsotype were identical or nearly identical at the genome level, with some exceptions. Two dominant subclones, clade 3a, and clade 4a, were responsible for the hospital-wide dissemination. Genomic analysis further revealed nine resistance genes mobilized by eight unique cassettes. PFGE and whole-genome sequencing revealed that the C. striatum isolates studied were the result mainly of predominant clones spreading in the hospital. C. striatum isolates in the hospital progressively acquired resistance to antimicrobial agents, demonstrating that isolates of C. striatum may adapt rapidly through the acquisition and accumulation of resistance genes and thus evolve into dominant and persistent clones. These insights will be useful for the prevention of C. striatum infection in hospitals.Entities:
Keywords: Corynebacterium striatumzzm321990; multidrug resistance; pulsed-field gel electrophoresis; transmission; whole-genome sequencing
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Year: 2019 PMID: 31315959 PMCID: PMC6711910 DOI: 10.1128/JCM.00683-19
Source DB: PubMed Journal: J Clin Microbiol ISSN: 0095-1137 Impact factor: 5.948
FIG 1Ward distribution of Corynebacterium striatum isolates. The pies illustrate pulsotype proportions of isolates recovered from each inpatient building. Rectangles illustrate unit and isolation date distributions of 9 dominant pulsotypes of 192 Corynebacterium striatum isolates. Others include all pulsotypes except the 9 dominant ones. ICU, Intensive Care Unit; CCU, Cardiac Care Unit; RCU, Respiratory Care Unit.
FIG 2Phylogenetic relationships of 91 Corynebacterium striatum isolates based on core genome SNPs. The dark-purple-shaded part indicates isolates of clade 1, the green-shaded part indicates isolates of clade 2, the light-purple-shaded part indicates isolates of clade 3, and the orange-shaded part indicates isolates of clade 4. The information of isolate identifications, isolation unit, isolation time, pulsotypes, resistance pattern, resistance genes, and ARGs are listed to the right of the genome tree. The number on the branches corresponds to the lengths (number of SNPs) generated by the maximum-likelihood algorithm.
FIG 3Distribution of group-specific SNPs within the two dominant clades. SNPs of each group are shown in Table S3, including SNP groups I to XI.
FIG 4Genomic context of macrolide, lincosamide, tetracycline, and aminoglycoside resistance. Reference sequence from Tn5432, that of ermX, known to mediate macrolide and lincosamide resistance (38). Maps of mobile elements containing resistance genes are shown in ARGs, with ermX in yellow, tetW in red, aminoglycoside-modifying enzyme (AME) genes in green, insertion sequences in blue, and opening reading frames in black. Unlabeled arrows indicate hypothetical proteins.