Comparative pathogenomics and in silico analysis of energy metabolism in Acinetobacter baumannii ST195 and novel Turkish isolates encoding blaOXA-23, blaOXA-66, and blaOXA-852

Acinetobacter baumannii is a significant hospital-acquired pathogen recognized for its antibiotic resistance and environmental durability. The present study investigates the genomic and metabolic characteristics of Turkish A. baumannii isolates (ST195 and novel sequence type) using whole-genome sequencing, comparative pathogenomics, and phenotypic assays. Genomic analyses demonstrated significant horizontal gene transfer, phage integration (Salmon_SSU5, Acinet_Bphi_B1251), and genomic islands enriched with resistance and virulence genes. ST195 (T3) exhibited meropenem susceptibility (MIC ≤ 0.125 µg/mL) despite harboring bla OXA-23, linked to adeN efflux regulator loss. In contrast, colistin resistance in T3 was correlated with putative lpxA/C/D mutations causing LPS deficiency. Virulence profiling identified conserved systems for adherence ( OmpA ), biofilm formation ( bap , csuABCDE ), and iron acquisition (acinetobactin), while capsule heterogeneity appeared to affect immune evasion. Metabolic reconstruction highlighted nitrogen and sulfur assimilation, as well as ethanol catabolism, which facilitate survival under host stress. Resistome analysis linked bla OXA -852 , adeFGH , and armA to resistance against carbapenems and aminoglycosides, while transposase-mediated frameshift mutations accounted for amikacin susceptibility in T3 despite the presence of APH(3’)-VIa . The open pangenome (6,402 genes, 41.9% core) reflected adaptive genomic plasticity. This study highlights the importance of genomic diversity, metabolic flexibility, and regulatory mutations in influencing A. baumannii resistance and virulence. It also identifies potential metabolic and virulence-related features that may guide future therapeutic and anti-virulence strategies.