# Genomic profiling of Elizabethkingia anophelis clinical isolates from a Shanghai hospital: phylogenetic divergence coexists with heterogeneous antibiotic resistance and virulence determinants

**Authors:** Jiasheng Xiong, Tiantian Han, Jingjing Hu, Yitian Wu, Xiaoyan Huang, Dianyu Yang, Weiwei Hou, Yan Lin

PMC · DOI: 10.3389/fmicb.2025.1751256 · 2026-01-16

## TL;DR

This study analyzes six E. anophelis strains from Shanghai, revealing diverse antibiotic resistance and virulence traits, with minocycline as a potential treatment option.

## Contribution

The study identifies phylogenetic divergence and heterogeneous resistance/virulence traits in E. anophelis clinical isolates from Shanghai.

## Key findings

- All isolates showed resistance to β-lactams, fluoroquinolones, carbapenems, and aminoglycosides but remained susceptible to minocycline.
- Phylogenetic analysis revealed two distinct clusters with different geographic affinities.
- Strain EA5 exhibited unique genetic signatures, including altered gene expression and resistance profiles.

## Abstract

Elizabethkingia anophelis (E. anophelis) has emerged as a multidrug-resistant pathogen with limited therapeutic options. This study aimed to characterize antimicrobial resistance mechanisms and virulence determinants in six clinical isolates from Shanghai, China, to inform evidence-based treatment strategies.

Six strains were isolated from hospitalized patients (five community-acquired, one healthcare-associated) between September–November 2023. Antimicrobial susceptibility testing followed CLSI M100 guidelines. Whole-genome sequencing employed hybrid Illumina/PacBio approaches. Phylogenetic relationships were determined through 16S rRNA gene sequence analysis using the Neighbor-Joining method. Antimicrobial resistance genes and virulence factors were annotated using the Comprehensive Antibiotic Resistance Database (CARD) and Virulence Factor Database (VFDB), with relative gene abundance quantified via a TPM-like (transcripts per million-like) method.

All isolates exhibited resistance to β-lactams, fluoroquinolones, carbapenems, and aminoglycosides, but retained minocycline susceptibility (MIC ≤1 μg/mL). Phylogenetic analysis revealed two distinct clusters: Cluster I (EA1, EA3, EA6) aligning with East/Southeast Asian isolates, and Cluster II (EA2, EA4, EA5) showing diverse geographic affinities. Five core resistance mechanisms were identified: antibiotic efflux, antibiotic target alteration, antibiotic inactivation, antibiotic target replacement, and reduced permeability to antibiotics. Virulence determinants included bacterial movement, exotoxin production, biofilm formation, immune regulation, and effector delivery systems. Strain EA5 exhibited unique signatures, including absence of cesH, unique sigE expression, elevated AAC(6′)-Iad/aadS and reduced qacL/OmpA.

This study reveals phylogenetically divergent E. anophelis lineages in Shanghai with extensive multidrug resistance but preserved minocycline susceptibility. Findings support minocycline-based therapy, enhanced diagnostics, and regional surveillance networks for strain monitoring.

Diagram showing various traits of a mosquito-related organism. Top left depicts morphological traits with petri dishes. Top right illustrates resistance mechanisms like efflux and permeability. Bottom left shows a phylogenetic tree. Bottom right highlights virulence factors, including exotoxin production and biofilm formation.

## Linked entities

- **Genes:** SIGE (sigma factor E) [NCBI Gene 832477], ompa (olfactory marker protein a) [NCBI Gene 574006]
- **Chemicals:** minocycline (PubChem CID 54675783), carbapenems (PubChem CID 134085)
- **Species:** Elizabethkingia anophelis (taxon 1117645)

## Full-text entities

- **Chemicals:** minocycline (MESH:D008911), carbapenems (MESH:D015780), beta-lactams (MESH:D047090), fluoroquinolones (MESH:D024841), aminoglycosides (MESH:D000617)
- **Species:** Elizabethkingia anophelis (species) [taxon 1117645], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12855470/full.md

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Source: https://tomesphere.com/paper/PMC12855470