Evidence map›Paper›PMID 42401803›Full record

ArticleBMC genomics2026

A genome-wide association study to identify the genetic loci underlying carbapenem resistance in Acinetobacter baumannii.

Gurprit Sekhon, Balvinder Singh

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Article in BMC genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Gurprit SekhonBioinformatics Centre (BIC), CSIR Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Balvinder SinghBioinformatics Centre (BIC), CSIR Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India. balvinder.singh@csir.res.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCarbapenem-resistant Acinetobacter baumannii (CRAB) presents a significant public health concern, and is recognized as a key contributor to the global antimicrobial resistance (AMR) crisis. This study applied a bacterial genome-wide association study (bGWAS) framework to identify genetic factors beyond the canonical carbapenemase OXA-23, that may contribute to carbapenem resistance.

methodsA. baumannii isolates with publicly available whole-genome sequencing (WGS) data and carbapenem-specific antimicrobial susceptibility testing (AST) results were compiled (n = 1,601). Unitigs were extracted from de novo assemblies, and single-nucleotide polymorphisms (SNPs) were called from raw sequence reads mapped to seven selected reference genomes. The unitig- and SNP-based genome-wide association analyses were carried out, including conditional analyses based on the known resistance determinants. Structural analysis was performed for the select candidate mutations.

resultsThe population was highly clonal and comprised ten lineages, including three predominantly resistant lineages (ST1, ST2, and ST32). Known CRAB-associated loci, including OXA-23, the RND efflux pump regulator AdeL, and OXA-66 variants (Ile129Leu and Leu167Val), were readily identified. Structural analysis of mutations identified outer-membrane proteins as potential candidate loci, however these loci were not supported in the conditional analyses across all reference genomes. The candidate loci supported in the conditional analysis across reference genomes included an amino acid substitution in a LysR-type regulator adjacent to the biofilm-associated operon pgaABCD, and an intergenic substitution located between enzymes involved in LPS remodeling.

conclusionsOXA-23 is the major determinant of carbapenem resistance in A. baumannii. Additional resistance mechanisms may become significant in the absence of OXA-23, including efflux pump regulation (AdeL), membrane permeability (OprD, DcaP), lipopolysaccharide (LPS) transport (PqiB), LPS remodeling (acyltransferase, glycosyltransferase), and biofilm formation (LysR). Integration of the conditional analysis based on known resistance determinants and a multi-reference mapping framework may improve the detection and prioritization of candidate associations.

Indexed as

Acinetobacter baumanniiCarbapenemsDrug Resistance, BacterialGenetic LociGenome-Wide Association StudyAnti-Bacterial AgentsBacterial Proteinsbeta-LactamasesGenome, BacterialMicrobial Sensitivity TestsPolymorphism, Single NucleotideWhole Genome SequencingAnti-Bacterial AgentsBacterial Proteinsbeta-LactamasesCarbapenemsAcinetobacter baumanniiBacterial GWAScarbapenem resistanceCRABGenome-wide association studyMutations

Identifiers

PMID42401803
PMCPMC13617891

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.