Nanopore sequencing captures first in-patient evolution of vancomycin-resistant E. faecium in New Zealand | LC 25

Biography

Dr Rhys White MASM, MRSNZ, is a computational biologist specialising in microbial genomics. Rhys earned his BSc (Hons) from Cardiff University and his PhD from The University of Queensland. His research addresses pathogen transmission, outbreak detection, and real-time genomic surveillance.

Rhys has worked in teams that have made contributions to public health by investigating the genomics of Chlamydia, Escherichia coli, Clostridioides difficile, Klebsiella variicola, and Staphylococcus aureus. His work advances the understanding of pathogen evolution and its application to infection control.

Abstract

Vancomycin-resistant Enterococcus faecium (VREfm) is a critical healthcare-associated pathogen with limited treatment options. Monitoring often targets VREfm; however, tracking vancomycin-susceptible E. faecium (VSEfm) can uncover early antibiotic resistance acquisition events, providing actionable insights for infection control.

At Wellington Regional Hospital, a decentralised whole-genome sequencing system, using Oxford Nanopore Technologies, integrates real-time genomic surveillance into routine workflows. Using the portable MinION device, this approach delivers actionable data on genotypic resistance and potential transmission events within hours.

Between January 2022 and November 2024, 177 VSEfm and 11 VREfm genomes were sequenced from hospital inpatients across the lower North Island. In August 2023, sequencing uncovered a distinct VSEfm cluster spanning two hospitals, comprising 33 genomes by November 2024 (median pairwise distance: 12 non-recombinogenic single-nucleotide variants (SNVs), interquartile range: 8–16).

Within this cluster, a significant event occurred in October 2024: a patient colonised with VSEfm developed a VREfm strain following vancomycin treatment. These two strains, sampled 54 days apart, were almost indistinguishable at the core genome (1 SNV). Sequencing pinpointed the acquisition of the vanB operon via a mobile Tn1549-like element, integrated into the E. faecium chromosome.

This genomic surveillance revealed resistance acquisition that would otherwise have gone unnoticed. Without this system, the VREfm would have been treated as a standalone case, obscuring its origin from the patient’s prior VSEfm colonisation.

These findings underscore the importance of proactive VSEfm monitoring to reveal hidden vulnerabilities in infection control practices and prevent the emergence of highly resistant pathogens that may have significant clinical and public health consequences.