Background
Acinetobacter baumannii is a multidrug-resistant bacterium responsible for severe
infections, particularly in hospital settings. Its resistance is driven by enzymatic genes
such as those encoding beta-lactamases and carbapenemases, which degrade
antibiotics, and non-enzymatic genes that modify mechanisms like efflux pumps and
membrane permeability, further enhancing its defence against treatments. Together,
these factors allow A. baumannii to thrive in clinical environments, complicating
infection management.
Objective
This study aimed to explore the relationships between beta-lactamases,
carbapenemases, efflux pumps, and membrane permeability changes, to understand
their collective contribution to A. baumannii's multidrug resistance.
Materials and Methods
Among 300 clinical isolates from urine, blood, wounds, and burns, 25 (8.33%) were
identified as A. baumannii. These included 8% from urine, 12% from blood, and 40%
each from wound and burn swabs.
all specimens were taken from patients who have different symptoms in
hospital of Al-Hilla Teaching Hospital/ Babylon. The research was
carried out through the period January and June 2024. Bacterial identification was
conducted using the VITEK-2 system and HI-Chromoagar® A. baumannii. Enzymatic
genes were detected using conventional PCR, while non-enzymatic genes were
analyzed via RT-qPCR.
Results
Molecular analysis revealed the presence of beta-lactamase (blaOXA-51, blaOXA-23)
and metallo-beta-lactamase genes (blaVIM, blaIMP), with high antibiotic resistance
rates. Gene expression analysis highlighted efflux pump upregulation (adeB) and
altered permeability (CarO), reinforcing multidrug resistance mechanisms.
Conclusion
The combined action of enzymatic and non-enzymatic resistance genes in A.
baumannii presents a significant treatment challenge, necessitating multi-target
therapeutic approaches.