The Presence of Plasmid-Mediated Quinolone Resistance Genes in Pseudomonas Aeruginosa Strains Collected from Clinical Samples in Al-Al Diwaniyah City

Document Type : New and original researches in the field of Microbiology.

Authors

Department of Medical Microbiology, College of Medicine, University of Kerbala, Kerbala, Iraq

Abstract

Background: The growing challenge of antibiotics resistances caused by Pseudomonas aeruginosa (P. aeruginosa, an important opportunistic pathogen) is one of the global healthcare issues. For epidemiological purpose, the identification of resistance genes is crucial. Objectives: The present study aims to determine the prevalence of PMQR encoding genes (qnr-A, qnr-B) phenotypically and genotypically in P. aeruginosa to determine epidemiological prevalence of these genes in Al-Diwaniyah city. Methodology: The study identified P. aeruginosa isolates from wounds and burns exudates, as well as urine samples from urinary tract infections (UTI) by biochemical characterization and VITEK 2 system. Conventional PCR was used to detect the presence of these genes. Results: Burns had a greater prevalence of P. aeruginosa (67.44%) than wounds (20.93%) and UTIs (11.63%). Antibiotic resistance analysis showed that thoroughly drug-resistant (XDR) bacteria predominated in burn infections (72.4%), wound infections (61%), and UTIs (66.7%). Molecular investigation showed that qnr-B and qnr-A are the most common resistance determinants in clinical isolates (97.91%). Antibiotic resistance patterns in wound, burn, and UTI infections were variable, but qnr-A and qnr-B genes showed that wound and burn cases with positive expressions had significantly increased MDR and XDR resistances. Positive expression of the qnr-A and qnr-b genes was associated with increased antibiotic resistance in all infection types, with substantial differences. Antibiotic susceptibility and gene expression studies for P. aeruginosa showed that resistant isolates have consistently high frequencies of positive gene expressions for these genes, especially for Imipenem and Meropenem. All isolates were Nalidixic acid-resistant and expressed these genes more. Only a few P. aeruginosa isolates are MEROPENEM-resistant intermediates. P. aeruginosa was responsive to all antibiotics except Nalidixic Acid. Our results demonstrate a varied correlation between antibiotic susceptibility and infection type, with statistically significant differences. Conclusion: This study demonstrate a predominance of plasmid-mediated fluoroquinolone resistance genes in the examined isolates. It is advisable to optimize fluoroquinolone utilization to maintain their efficacy against multidrug-resistant bacteria.

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