Spectral analysis software identified significant species-specific peaks to create reference masses for efficient and accurate identification of Elizabethkingia species, providing accurate information for clinical treatment of Elizabethkingia infections.

Background MDR Elizabethkingia anophelis strains are implicated in an increasing number of healthcare-associated infections worldwide, including a recent cluster of E. anophelis infections in the Midwestern USA associated with significant morbidity and mortality. However, there is minimal information on the antimicrobial susceptibilities of E. anophelis strains or their antimicrobial resistance to carbapenems and fluoroquinolones. Objectives Our aim was to examine the susceptibilities and genetic profiles of clinical isolates of E. anophelis from our hospital, characterize their carbapenemase genes and production of MBLs, and determine the mechanism of fluoroquinolone resistance. Methods A total of 115 non-duplicated isolates of E. anophelis were examined. MICs of antimicrobial agents were determined using the Sensititre 96-well broth microdilution panel method. QRDR mutations and MBL genes were identified using PCR. MBL production was screened for using a combined disc test. Results All E. anophelis isolates harboured the blaGOB and blaB genes with resistance to carbapenems. Antibiotic susceptibility testing indicated different resistance patterns to ciprofloxacin and levofloxacin in most isolates. Sequencing analysis confirmed that a concurrent GyrA amino acid substitution (Ser83Ile or Ser83Arg) in the hotspots of respective QRDRs was primarily responsible for high-level ciprofloxacin/levofloxacin resistance. Only one isolate had no mutation but a high fluoroquinolone MIC. Conclusions Our study identified a strong correlation between antibiotic susceptibility profiles and mechanisms of fluoroquinolone resistance among carbapenem-resistant E. anophelis isolates, providing an important foundation for continued surveillance and epidemiological analyses of emerging E. anophelis opportunistic infections. Minocycline or ciprofloxacin has the potential for treatment of severe E. anophelis infections.

ObjectivesSeveral Elizabethkingia species often exhibit extensive antibiotic resistance, causing infections associated with severe morbidity and high mortality rates worldwide. In this study, we determined fluoroquinolone susceptibility profiles of clinical Elizabethkingia spp. isolates and investigated the resistance mechanisms.MethodsIn 2017–2018, 131 Elizabethkingia spp. isolates were recovered from specimens collected at tertiary care centers in northern Taiwan. Initial species identification using the Vitek MS system and subsequent verification by 16S rRNA sequencing confirmed the presence of Elizabethkingia anophelis (n = 111), E. miricola (n = 11), and E. meningoseptica (n = 9). Fluoroquinolone susceptibility was determined using the microbroth dilution method, and fluoroquinolone resistance genes were analyzed by sequencing.ResultsAmong Elizabethkingia spp. isolates, 91% and 77% were resistant to ciprofloxacin and levofloxacin, respectively. The most prevalent alterations were two single mutations in GyrA, Ser83Ile, and Ser83Arg, detected in 76% of the isolates exhibiting fluoroquinolone MIC between 8 and 128 μg/ml. Another GyrA single mutation, Asp87Asn, was identified in two quinolone-resistant E. miricola strains. None of the isolates had alterations in GyrB, ParC, or ParE. We developed a high-resolution melting assay for rapid identification of the prevalent gyrA gene mutations. The genetic relationship between the isolates was evaluated by random amplified polymorphic DNA PCR that yielded diverse pulsotypes, indicating the absence of any temporal or spatial overlap among the patients during hospitalization.ConclusionOur analysis of fluoroquinolone-resistant Elizabethkingia spp. isolates provides information for further research on the variations of the resistance mechanism and potential clinical guidance for infection management.

No abstract