AdeG efflux pump as the main Tigecycline resistance in Acinetobacter baumannii
https://doi.org/10.1016/j.genrep.2020.100689
- aStudent Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
- bCellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
- cZoonoses Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
- dLiver and Digestive Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
- eDepartment of Microbiology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran
- fDepartment of Microbiology and Virology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract
Background and aims
Infection and outbreaks caused by tigecycline-resistant Acinetobacter baumannii strains have reported worldwide. However, the relative contribution of the efflux pump data in the clinical settings is limited. In the present study, we investigated the expression of tigecycline resistance genes.
Method and materials
In this cross-sectional study a total of 46 A. baumannii isolates were collected from clinical samples in three medical centers. Antibiotic susceptibility testing, by broth micro-delusion (BMD), and the relative expression of adeB, adeG, adeJ, and abeM, by semi-quantitative PCR (semi-qPCR) were quantified. The effect of the efflux pump inhibitor (EPI) was evaluated.
Results
Of 119 Acinetobacter isolates from three university hospital centers, 46 A. baumannii isolates were detected. The results of BMD susceptibility testing showed that >67.4% of isolates had MIC ≤4. The MIC of tigecycline in the presence of EPI decreased in 38.7% of resistant isolates. The results of semi-qPCR showed that the highest expression of efflux genes was related to adeG.
Conclusion
The results of this study showed a high prevalence of tigecycline resistance in A. baumannii, the main cause of which was the increased expression of RND efflux pumps and at the top adeG. This resistance is probably due to point mutations in the regulatory genes of these efflux pumps.