Biology subjects

Pulmones, R.

Publications and source records attributed to Pulmones, R..

3 recordsLinked to original sources

bioRxiv2026

In vivo de-amplification of a multi-resistance pseudo-compound transposon in Escherichia coli

The rapid expansion of antimicrobial resistance (AMR) among Gram-negative pathogens presents a major clinical challenge, particularly in vulnerable populations such as infants. The dissemination of resistance is often mediated by mobile genetic elements (MGEs) that can mobilise antimicrobial resistance genes (ARGs) both within and between genomes. The insertion sequence (IS) IS26, is a MGE with the ability to replicate itself and associated ARGs, create translocatable units (TU), and produce tandem arrays of ARGs. Here we present the 18-week in vivo evolution of a community-acquired multi-drug resistant (MDR) Escherichia coli colonising an infant gut, characterised by a de-amplification of an IS26-mediated tandem array of ARGs. The hybrid-assembled ancestral and descendant strain genomes show an evolutionary rate of 10.22 SNPs per genome per year. Independent analysis of the hybrid genome assembly, and of Oxford Nanopore Technologies (ONT) and Illumina read-mapping support the existence of at least five copies of a TU (Tn3-like(tnpA)-tetR-tetA-yedA-{Delta}Tn1721(tnpA) -IS26-aac(6)-Ib-cr-blaOXA-1-{Delta}catB3-IS26) in the ancestor and only one in the descendant. Despite de-amplification, no change in fitness (p = 0.275) and piperacillin-tazobactam susceptibility (TZP) was observed. In contrast, gentamicin susceptibility increased, in the absence of known associated mutations. This study provides insight into IS26-mobility dynamics in vivo and their implications for AMR, within the rapidly changing environment of the neonatal gut.

microbiology↗

bioRxiv2026

A citywide metagenomic analysis reveals surface-specific microbiome and resistome patterns in outdoor urban environments across Liverpool, UK.

Urbanisation is rapidly increasing worldwide, with increasing attention focused on its consequences for human populations and the environment. Despite the importance of outdoor urban environments for biodiversity and human wellbeing, their microbial ecology remains poorly characterised, particularly in relation to emerging microbial threats including antimicrobial resistance (AMR). Here, we present a citywide metagenomic study of outdoor public surfaces across Liverpool, United Kingdom, examining microbial community composition, diversity, and antimicrobial resistance gene (ARG) distribution across five distinct surface types. We show that patterns of human activity and surface use strongly influence both microbial community structure and AMR signatures in outdoor urban environments. Touchpoints were enriched for human-associated taxa and exhibited the highest overall resistome burdens, whereas Pathway and Waterside niches showed no strong taxonomic enrichment and exhibited low ARG prevalence. Refuse surfaces showed mixed patterns, characterised by sporadic but occasionally high-abundance ARG detections. Soil harboured the most distinct microbial communities but showed minimal ARG prevalence, which may partly reflect the limited representation of environmental taxa in current ARG databases. This study provides a baseline for understanding how urban infrastructure and behaviour shape microbial and resistance landscapes, and highlights the value of outdoor metagenomic surveillance for future environmental and public health research.

microbiology↗

bioRxiv2025

From Colonisation to Invasion: Genomic and Phenotypic Comparison of Faecal and Bloodstream Isolates from the same patients

Gram-negative bloodstream infections (GNBSI) carry a significant global health burden. Escherichia coli and Klebsiella pneumoniae are the two most common causes of healthcare-associated GNBSI, which may arise from gastrointestinal tract (GIT) colonisation. Understanding genomic and phenotypic adaptations that underpin transition from GIT colonisation to invasive bloodstream infection could improve understanding of pathogenesis. This study identified linked faecal and blood isolates from children with healthcare-associated GNBSI caused by E. coli and K. pneumoniae. Linked pairs were compared for antimicrobial resistance, biofilm formation, and underwent comparative genomic analysis via whole-genome sequencing, comparative average nucleotide identity (ANI) and core genome single nucleotide polymorphism (SNP) analysis. Five isolate pairs (three E. coli, two K. pneumoniae) showed high relatedness, supporting GIT origin of bloodstream infection. Isolates within pairs had identical virulence genes whereas phenotypic assays revealed changes in antimicrobial susceptibility, with one pair undergoing changes in resistance gene profiles, and increased biofilm formation in 4/5 isolates. This study provides insight into within-host evolution from gastrointestinal colonisation to bloodstream invasion in Gram-negative pathogens. Convergence on metabolic adaptation and biofilm formation suggests these traits may be advantageous in healthcare-associated GNBSI. Further studies involving larger cohorts alongside functional validation of mutations are needed to better understand GNBSI pathogenesis.

microbiology↗