Biology Research Center, Systems Biology and Poisoning Institute,
Baqiyatallah University of Medical Sciences, Tehran, Iran.
2 Department of Microbiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
3 Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
4 Department of Microbiology, Faculty of Medicine, Babol University of medical sciences, Babol, Iran.
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(https://creativecommons.org/licenses/by-nc/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
is an important opportunistic pathogen, responsible for approximately
10% of all gram-negative nosocomial infection. The aim of this study
was to determine aminoglycoside and quinolone resistance genes and
their antimicrobial susceptibility profile in the clinically A. baumannii. In this cross-sectional study, a total of 100 nonduplicative A. baumannii
isolates were collected from different clinical samples. Antimicrobial
susceptibility test was performed by disk diffusion method. QnrA, anrB, qnrS, aac(3)-IIa, and aac(6′)-Ib
genes were identified using PCR method. The results of antibiotic
susceptibility test showed that polymyxin B was the most effective
antimicrobial against A. baumannii.
97%, 95% and 82% of isolates were resistant to cefepime, ceftriaxone,
and amikacin, respectively. The molecular distribution of aac(3)-IIa, aac(6′)-Ib, and qnrA genes were 45%, 50%, and 50% of isolates, respectively. However, qnrB and qnrS genes could not be detected in any strain. This study showed that polymyxin B was the best drug against A. baumannii clinical
isolates. This data is also valid for polymyxin E (colistin), which is
mostly used in clinics. There is a high level of resistance genes among
clinical A. baumannii
isolates. This high prevalence rate highlights the necessity for the
development of rapid diagnostic assays and continuous monitoring of
Materials and Methods
|Table 1. PCR primers and annealing temperatures used in this study.|
|Table 2. Antibiotics resistance profile among A. baumannii isolates.|
|Figure 1. A) PCR amplification of the aac(3)-IIa gene. Lane M: Ladder (100 bp), lane Cont-: negative control, lane Cont+: positive control (740bp); lane 1, 6, and 7: negative results and lane 2, 3, 4, and 5: positive results. B) PCR amplification of the aac(6′)-Ib gene. Lane M: Ladder (100 bp), lane Cont-: negative control, lane Cont+: positive control (482bp); lane 1-7: positive results. C) PCR amplification of the qnrA gene. Lane M: Ladder (100 bp), lane Cont-: negative control, lane Cont+: positive control (649bp); lane 1-4, 5, and 7: positive results, lane 5: negative result.|