Comparative Genomics of Multidrug-Resistant and Extensively Drug-Resistant Acinetobacter Baumannii Clinical Isolates from an Intensive Care Unit in Northeastern Brazil

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Abstract

Acinetobacter baumannii is an opportunistic pathogen linked to healthcare-associated infections and the dissemination of multidrug-resistant phenotypes in critical hospital settings. In this study, we performed a comparative genomic analysis of clinical isolates identified as A. baumannii by routine hospital microbiology, obtained from an intensive care unit in Northeastern Brazil and classified as susceptible (SEN), multidrug-resistant (MDR), or extensively drug-resistant (XDR). Fifteen isolates were subjected to whole-genome sequencing; after quality control, 14 genomes were included in the main comparative analyses. Genome assembly metrics, functional composition, pangenome, resistome, virulome, Pasteur MLST, core-genome phylogeny, phenotype–genotype concordance, and FastANI-based taxonomic refinement were evaluated. MDR and XDR isolates carried a higher burden of antimicrobial resistance (AMR) genes than SEN isolates. Pangenome analysis revealed a conserved core genome combined with variable accessory content, whereas the virulome was relatively conserved across phenotypic groups. Quinolone resistance-determining region (QRDR) mutations in gyrA and/or parC were detected in ciprofloxacin-resistant isolates, supporting the role of chromosomal mechanisms in fluoroquinolone resistance that may not be captured by analyses restricted to acquired resistance genes. FastANI analysis further revealed taxonomic discrepancies in two susceptible isolates, highlighting the complementary value of WGS for hospital surveillance and taxonomic refinement within the Acinetobacter calcoaceticus–baumannii complex. Overall, our findings indicate that antimicrobial resistance in these clinical isolates is a multifactorial phenomenon shaped by clonal diversity, accessory genome variation, AMR gene burden, chromosomal resistance mechanisms, and taxonomic complexity within the ACB complex.

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