Molecular Characteristics and Antimicrobial Susceptibility Profiles of Elizabethkingia Clinical Isolates in Shanghai, China

Abstract

Purpose

To investigate molecular characteristics and antimicrobial susceptibility profiles of clinical isolates of Elizabethkingia in Shanghai, China.

Methods

Elizabethkingia isolates were collected in a university-affiliated hospital in 2012–2015 and 2017–2018. They were re-identified to species level by 16S rRNA gene and species-specific gene sequencing. Antimicrobial susceptibility testing, screening for metallo-beta-lactamase production, identification of antimicrobial resistance genes and pulsed-field gel electrophoresis (PFGE) were performed.

Results

Among 52 Elizabethkingia isolates, E. anophelis was the most prevalent species (67.3%), followed by E. meningoseptica (26.9%). High carriage rates of bla_CME, bla_BlaB and bla_GOB genes were consistent with the poor in vitro activity of most β-lactams including carbapenems. Nevertheless, β-lactamase inhibitors increased susceptibility rates significantly for cefoperazone and piperacillin. Susceptibility rates for minocycline, tigecycline, rifampin and levofloxacin were 100%, 78.8%, 76.9% and 71.2%, respectively. Ser83Ile or Ser83Arg substitution in the DNA gyrase A unit was associated with resistance to fluoroquinolones. MIC₅₀/MIC₉₀ values of vancomycin and linezolid were 16/16 mg/L and 16/32 mg/L, respectively. Molecular typing showed twenty-one different types of PFGE and more than one indistinguishable isolates were observed in each of the eight subtypes.

Conclusion

Tetracyclines, tigecycline, β-lactam/β-lactamase inhibitor combinations, rifampin and fluoroquinolones demonstrated high rates of in vitro activity against clinical isolates of Elizabethkingia. Both genetic diversity and clonality were observed from this health-care facility. Our report provides potential alternative treatment options for Elizabethkingia infections.

Keywords:

• Elizabethkingia
• antimicrobial susceptibility
• molecular typing
• multidrug resistance
• resistant mechanism

Acknowledgments

The authors thanked Dr. Yohei Doi for his critical review of the manuscript. The authors also thanked Mengyun Yin, Renru Han, Li Ding and Pei Li at Institute of Antibiotics for assistance and collaboration in laboratory work. This work was supported by grants from the National Natural Science Foundation of China (grant numbers 81872909 and 81673479). The funder had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics Approval

Verbal informed consent of patients was obtained after the approval of the Ethics Committee of Huashan Hospital, Fudan University, China (approval number: KY2019-544). The patient data were analyzed in anonymity.

Disclosure

The authors report no conflicts of interest in this work.