Acinetobacter baumannii relies on biofilms for antibiotic resistance, but the role of planktonic aggregates in drug tolerance is uncharacterized. We studied 103 clinical isolates to explore how the RND efflux pump gene adeG regulates aggregation. Non-MDR strains (with RND deletions) formed aggregates more frequently (13.79%, 4/29) than MDR strains (1.35%, 1/74), driven by residual RND efflux activity (not just deletions). adeG deletion induced 1–2 mm aggregates in a strain with combined adeR/ΔadeABC defects (via upregulated adhesion genes/hydrophobicity) but not in one with only ΔadeC. Aggregates boosted antibiotic tolerance (2–4-fold higher survival vs. disaggregated/parental strains) via metabolic dormancy (5-fold lower ATP), maintained growth in human serum, and promoted persistent bacteremia in immunosuppressed mice. Proteinase K disrupted aggregates, confirming protein matrices’ role. These findings identify planktonic aggregates as pivotal adaptive and virulence-related targets for combating refractory non-MDR A. baumannii infections while also revealing an association between adeG-related genetic contexts and aggregate formation in the bacterium.