Mutations in gyrA and parC genes in fluoroquinolone-resistant Acinetobacter baumannii that causes hospital acquired infection | ||||
| Microbes and Infectious Diseases | ||||
| Article 28, Volume 4, Issue 2, May 2023, Page 590-600 PDF (1.22 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/mid.2023.183097.1435 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Marwa S. Taha 1; Sarah M. Shoeib  2; Marwa A. Abdelwahab 1
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| 1Department of Medical Microbiology and Immunology, Faculty of Medicine, Tanta University, Egypt | ||||
| 2Department of Clinical Pathology, Faculty of Medicine, Tanta University | ||||
| Abstract | ||||
| Background: Acinetobacter baumannii, are involved in hospital- acquired infections and are increasingly developing resistance to fluoroquinolones, such as ciprofloxacin. The most common method of fluoroquinolone resistance is alteration in genes that encode DNA gyrase (gyrA) and topoisomerase IV (parC).Methods: We sought to isolate fluoroquinolone- resistant A. baumannii and search for changes in gyrA (Ser83Leu) and parC (Ser80Leu) loci by polymerase chain reaction- restriction fragment length polymorphism (PCR- RFLP).Results: We found that all 68 A. baumannii isolates that were part of this research were multidrug resistant and harbored gyrA and parC loci. Most isolates had ciprofloxacin minimal inhibitory concentrations of >128 μg/mL (50.8%). Mutations in gyrA were the most prevalent (47.45%), followed by parC mutations (33.9%) and combined mutations in both genes (23.7%).Conclusions: Single mutations in either gyrA (Ser83Leu) or parC (Ser80Leu) genes may be attributed to fluroquinolone resistance in A. baumannii. | ||||
| Keywords | ||||
| Acinetobacter baumannii; fluoroquinolone resistance; gyrA, parC; PCR-restriction fragment length polymorphism | ||||
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