Genomic and epidemiological identification of Pseudomonas aeruginosa transmission chains and in hospital ICUs

TL;DR

This study uses genomic data to track how Pseudomonas aeruginosa spreads in hospital ICUs, showing that contaminated sinks and patient-to-patient transmission are key sources of infection.

Contribution

The study introduces a 24 SNP genetic threshold for identifying transmission clusters and highlights the role of environmental reservoirs in ICU infections.

Findings

A 24 SNP threshold effectively identifies epidemiologically linked Pseudomonas aeruginosa strains.

Environmental reservoirs in ICU sink drains persist for nearly two years and contribute to infections.

Over 70% of environment-patient strain pairs show epidemiological linkage, indicating direct transmission.

Abstract

Pseudomonas aeruginosa (PA) is an opportunistic pathogen that poses a significant threat to hospitalized patients, particularly in intensive care units (ICUs) due to its ability to contaminate the environment and subsequently infect vulnerable patients. This study seeks to demonstrate that genomic data is an accessible, rapid, and robust genomic epidemiological tool that can be used in a clinical or diagnostic setting to improve our understanding of PA transmission dynamics and enhance infection prevention and control strategies.

We performed analysis on 2046 PA isolates recovered from patients and sink drains in seven hospital ICUs. We find that a pairwise genetic distance threshold of 24 SNPs best approximates the maximum expected divergence between clonal strains. The pairing of this genetic threshold and the ELS identifies 82 transmission clusters, encompassing 730 isolates, suggesting both environment-patient and patient-patient transmission. Our analysis identifies PA reservoirs in ICU sink drains that last nearly two years and transmission clusters that span multiple ICUs, indicating inter-hospital transmission or shared external reservoirs. Epidemiological linkage is identified for over 70% of genetically linked environment-patient strain pairs and 49% of genetically linked patient-patient strain pairs.

We find strong support for the use of a genetic threshold to identify epidemiologically linked strains. We find genomic evidence for persistent environmental reservoirs as sources of ICU-associated PA infection. This work underscores the importance of environmental monitoring and infection control measures to mitigate the risk posed by contaminated sinks and other environmental sources.

The online version contains supplementary material available at 10.1186/s13059-026-04005-1.

Figures