Antimicrobial Resistance and Virulence Profiles of Acinetobacter baumannii in Pediatric Healthcare-Associated Bacteremia.

BACKGROUND

Several factors play a role in the pathogenesis of Acinetobacter baumannii (A. baumannii). This study aimed to determine the virulence genes of A. baumannii isolated from healthcare-associated bacteremia (HAB) in pediatric patients, as well as their biofilm-forming ability and resistance to carbapenem antibiotics.

METHODS

One hundred isolates of A. baumannii from healthcare-associated bacteremia in children, collected be-tween January 2024 and January 2025, were subjected to biochemical identification using the API 20NE system, and confirmation of A. baumannii was performed by PCR targeting the blaOXA-51-like gene. Biofilm formation determination was quantified using the standard microtiter plate assay with crystal violet staining. Antimicrobial susceptibility testing was conducted using the Kirby-Bauer disc diffusion method on Mueller-Hinton agar. Genetic studies using the polymerase chain reaction (PCR) were performed to detect virulence-associated genes, including bap, surA1, pld, csuE, ompA, kps, and iron acquisition genes (basD, entE, and tonB) [17-22]. Screening for carbapenemase genes (blaOXA-23, blaOXA-24/40, blaOXA-58, blaNDM) was also conducted.

RESULTS

A. baumannii was able to form strong biofilm in 20%, intermediate biofilm in 30%, and weak biofilm in 25% of the isolates. All A. baumannii isolates contained the bap and surA1 genes (100%), the pld gene (84%), and the basD gene (79%).

CONCLUSIONS

The significant presence of bap and surA1 genes among all imipenem-resistant and biofilm-forming isolates highlights their central role in enhancing both virulence and antimicrobial resistance. Moreover, there are significant correlations between imipenem resistance, omp33-36, and blaOXA-40, emphasizing the combined contribution of altered membrane permeability and carbapenemase activity to resistance phenotypes. The association of biofilm formation with blaOXA-23 and basD genes further reflects a multifactorial resistance strategy.