Molecular Detection of papE Virulence Genes in Escherichia coli Isolated from Women with Urinary Tract Infection.

Background: Urinary Tract Infections (UTIs) are among the most prevalent bacterial infections in women, often caused by uropathogenic Escherichia coli (UPEC). The papE gene, a component of the P fimbriae operon, is recognised as a key virulence factor facilitating bacterial adhesion and colonization of uroepithelial cells. Objective: This study aimed to detect the presence of the papE virulence gene in clinical E. coli isolates obtained from women with UTIs using molecular methods. Methods: A total of 116 urine samples from women with clinically diagnosed UTIs were collected. E. coli isolates were identified using standard microbiological methods and confirmed by the VITEK® 2 Compact system. Genomic DNA was extracted from the isolates and PCR amplification of the papE gene was performed using gene-specific primers. Amplification products were analysed by electrophoresis on 1.5% agarose gels. Results: According to Sex Distribution: Out of the 116 clinical bacterial isolates, 41 (36.6%) were from male patients, while 71 (63.4%) were from female patients. The isolates’ resistance to quinolone antibiotics, which includes nalidixic acid, ciprofloxacin and levofloxacin, was at 82.5, 56.3 and 50%, respectively. Cephalosporins, which include cefoxitin, cefotaxime, ceftazidime, cefepime and ceftriaxone, had a resistance of 53.3, 60, 76.6, 66.6 and 53.3%, respectively, for each aforementioned antibiotic. The isolates’ resistance to carbapenems, which includes meropenem and imipenem, was at 22 and 35%, respectively. As for β-lactam combinations, which include Augmentin and piperacillin-tazobactam, the resistance was found to be at 60 and 40%. And as for the penicillin group of antibiotics that includes piperacillin, the resistance was found to be 46.6%. Tetracycline from the antibiotic group of the same name and chloramphenicol from the antibiotic group phenicol both had a resistance rate of 46.6%. Aztreonam, from the antibiotic group minocycline, had resistance at 73.3%. The isolates were capable of producing biofilms; 20 isolates (66.7%) were biofilm producers out of 30 isolates,7 isolates accounting for 35% were strong biofilm producers, while 8 isolates (40%) were moderate biofilm producers. The remaining 5 isolates, accounting for 25 % of the total isolates, were weak biofilm producers. Conclusions: The detection of the papE gene in clinical E. coli isolates highlights its potential role in UTI pathogenesis and underscores the importance of molecular surveillance of virulence factors in guiding therapeutic strategies. Future studies should explore the association of papE with antimicrobial resistance patterns and biofilm formation to develop targeted interventions.