Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.01.20.700532

Historical isolates provide insights into the evolution of Acinetobacter baumannii international clone 2 and its resistome

Abstract

Acinetobacter baumannii remains a pervasive nosocomial pathogen, with international clone 2 (IC2) being the most successful lineage. IC2 is often discussed as a singular entity, and the genomic factors behind its success over other lineages are poorly characterised. This study aimed to track genomic changes occurring around the emergence of IC2 and further determine the within-clone population structure. A set of historical A. baumannii isolates from the 1970s to early 2000s were long-read sequenced and assembled into high-quality chromosomes. These were then used to supplement publicly available A. baumannii genomes, producing a dataset of 1,281 chromosomes derived from isolates collected across six continents. A recombination-free phylogeny was produced and combined with antimicrobial resistance gene (ARG) presence/absence data. Analysis showed that IC2 began to emerge as the dominant lineage around 2005, which coincides with the acquisition of oxa23 and AbGRI3. Further, IC2 can be split into at least four distinct groups. Groups 1, 2, and 3 represent incremental evolution of the A. baumannii chromosome over time, while group 4 represents a separate evolutionary path distinct from the main IC2 lineage, which has recently been isolated at higher frequency. Significance statementCharacterising the evolution and population structure of antimicrobial-resistant bacterial pathogens is of key importance both for epidemiological monitoring and developing approaches to combat infections and their spread. Here, we use a unique collection of historical isolates to show that the major international clone in the WHO priority pathogen Acinetobacter baumannii is comprised of different, independent groups with individual antimicrobial resistance gene compliments. This highlights new areas for research to understand the clinical impact of the different groups and the drivers underlying the evolution and spread of epidemic clones of antimicrobial-resistance bacterial pathogens.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Neil, M., Grenier, F., Allard, N., Langridge, G. C., Castillo-Ramirez, S., Haraoui, L.-P., Evans, B. A.. 2026-01-20. Historical isolates provide insights into the evolution of Acinetobacter baumannii international clone 2 and its resistome. https://doi.org/10.64898/2026.01.20.700532

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Matrix-controlled emergence of biofilm architecture shapes antimicrobial survival

Biofilms are structured microbial communities whose extracellular matrix is widely regarded as a basis of their protection against antimicrobial compounds. Yet how matrix production by individual bacteria gives rise to collective architecture and antimicrobial protection remains poorly understood. Here, we systematically varied expression of the master biofilm regulator csgD in Salmonella enterica and found that increasing matrix production reorganizes biofilms from dense, isotropic packings into sparse, nematically aligned communities by altering cell-cell interactions. By combining experimentally measured biofilm architectures with reaction-diffusion modeling, we show that these structural changes produce distinct patterns of antimicrobial killing, ranging from preferential killing near the liquid-biofilm interface to more uniform killing throughout the community. Consequently, increasing matrix production unexpectedly reduces antimicrobial survival by shifting the biofilm into different transport regimes, while strain-specific physiological differences further modulate antimicrobial depletion. Rather than acting as a passive barrier, EPS therefore shapes antimicrobial susceptibility by reorganizing biofilm architecture and its transport properties. EPS thus provides a physical link between molecular regulation, collective architecture and antimicrobial survival, providing a quantitative framework for understanding how cellular matrix production generates emergent biofilm function.

microbiology↗

Mapping virulence-associated protein interaction networks reveals regulators of thermotolerance in Cryptococcus neoformans

Protein-protein interactions (PPIs) influence critical biological processes in pathogenic microorganisms, such as the human fungal pathogen, Cryptococcus neoformans. Fungal thermotolerance and stress response pathways are key virulence determinants that directly impact pathogen adaptation and survival and the infection process. To establish a comprehensive baseline of PPIs in C. neoformans and explore these interactions to infer functional roles for uncharacterized proteins, we applied size exclusion chromatography coupled with mass spectrometry to the secreted and cellular proteomes of the fungi. As a result, 216 and 1699 unique proteins were identified across 24 secretome and proteome fractions, respectively. The predicted secretome networks included expected proteins associated with vesicles and virulence, indicating a role in extracellular defense. Whereas the cryptococcal proteome highlighted interactions among proteins with defined roles in fungal virulence for protein stability and thermotolerance, including two previously uncharacterized proteins, CNAG_00287 and CNAG_05199, putatively involved in complex formation with heat-shock proteins (HSP). Based on sequence and structure homology, we propose that CNAG_00287 is a tetratricopeptide repeat-containing co-chaperone that modulates Hsp 70 activity and CNAG_05199 functions as a Hsp70. We validated the thermotolerance role of CNAG_00287 in heat-related stress, as its absence significantly impaired fungal growth in nutrient-limited media at 37 {degrees}C. Together, this work resolves virulence-associated PPIs within C. neoformans and reveals new molecular regulators of thermotolerance that underpin fungal pathogenicity.

microbiology↗

Environmental filtering and host identity collectively shape root-associated microbiomes of Ericaceae and ectomycorrhizal plants in fumarole fields

Background Symbiosis with microbes is a key strategy that has enabled plants to colonize extreme environments. Since the benefits conferred by root-associated microbes depend on both environmental conditions and host-microbe combinations, plant adaptation to harsh environments is closely linked to the assembly of root microbial communities. Understanding how environmental and host filtering jointly shape these communities is therefore fundamental to elucidating the mechanisms underlying plant adaptation to extreme environments. Results In this study, we investigated the differentiation of root-associated prokaryotic and fungal communities and individual operational taxonomic units (OTUs) across two contrasting habitats surrounding fumaroles, solfatara-field and forest-edge habitats, and six dominant Ericaceae and ectomycorrhizal plant taxa. Prokaryotic and fungal OTUs rarely exhibited strong preferences for both habitat and host identity. Instead, many of prokaryotic and fungal OTUs specialized to one of these niches, collectively generating root microbial communities differentiated by both factors. Nonetheless, striking specializations in habitat and host niches were observed in the fungal family Hyaloscyphaceae (Helotiales). To gain insight into the evolutionary basis of microbial specialization, we examined phylogenetic signals in preference phenotypes. The resulting weak phylogenetic signals in these preference phenotypes further suggest that this fungal clade has undergone substantial ecological divergence. Conclusion Overall, our findings indicate that root-associated microbial communities in extreme environments are assembled through the accumulation of microbial taxa specialized to either habitat or host, and that strong ecological specialization in fungi can arise with little phylogenetic constraint.

microbiology↗