Acinetobacter baumannii Global Clone-Specific Resistomes Explored in Clinical Isolates Recovered from Egypt

Acinetobacter baumannii (A. baumannii) is a highly problematic pathogen with an enormous capacity to acquire or upregulate antibiotic drug resistance determinants. The genomic epidemiology and resistome structure of 46 A. clinical isolates were studied using whole-genome sequencing. chosen based on reduced susceptibility at least three classes antimicrobial compounds initially identified MALDI-TOF/MS, followed by polymerase chain reaction amplification blaOXA-51-like genes. profiles determined broth microdilution assay. Multi-, extensive-, pan-drug was shown 34.8%, 63.0%, 2.2% the isolates, respectively. These most susceptible colistin (95.7%), amikacin, trimethoprim/sulfamethoxazole (32.6% each), while only 26.1% tigecycline. In silico multi-locus sequence typing revealed 8 Pasteur 22 Oxford types (STs) including four novel STs (STOxf 2805, 2806, 2807, 2808). majority belonged Global Clone (GC) 2 (76.4%), GC5 (19.6%), GC4 (6.5%), GC9 (4.3%), GC7 (2.2%) lineages. An extensive potentially conferring tested antimicrobials in silico. Of all known carbapenem genes, blaOXA-23 carried (69.6%), ISAba1-amplified blaADC (56.5%), blaNDM-1 blaGES-11 (21.7% blaGES-35 A significant correlation found between carO mutations, which evident 35 (76.0%) isolates. lower proportion noted for strains possessing both blaOXA-23- blaGES-11. Amikacin probably mediated armA, aac(6′)-Ib9, aph(3′)-VI, commonly coexisting GC2 No mutations pmrABC lpxACD operons colistin-resistant Tigecycline associated adeS (N268Y) baeS (A436T) mutations. While lineage-specific distribution some genes (e.g., alleles) evident, such as sul1, GCs. data generated here highlight contribution five GCs infections Egypt enable comprehensive analysis GC-specific resistomes, thus revealing dissemination gene encompassing