Relationship between antimicrobial resistance and virulence factors in uropathogenic Escherichia coli isolates from Ramadi, Iraq: phenotype and genotype identification

Abstract

Background: Uropathogenic Escherichia coli (UPEC) is the most predominant pathogen that causes severe urinary tract infections (UTIs). Their therapeutic options are limited due to the rising of antibiotic resistance. Objective: The aim of the study was to evaluate the level of antibiotic resistance profile, redundancy of virulence genes, and their correlation. Methods: 41 UPEC isolates were collected from patients diagnosed with UTI, identified by the standard microbiological analysis, and tested for susceptibility to 12 antibiotic agents using the Kirby-Bauer method. The ability of UPEC isolates to produce biofilm, hemolyze and cause clumping of blood was determined. Virulence genes were detected by PCR analysis. Results: The percentage of UPEC isolates was higher in females (78.1%) than in males (21.9%). UPEC isolates showed a high degree of resistance towards Ceftriaxone (90.2%), Cefepime (90.2%), Ciprofloxacin (82.9%), Levofloxacin (82.9%), and Trimethoprim-Sulfamethoxazole (80.4%). Biofilm formation (87.8%) and hemagglutinin activity (80.4%) were the most predominant virulence markers expressed in UPEC and showed a high degree of correlation with the antibiotic resistance profile. PCR analysis showed that fimH (85.3%) was the most prevalent gene detected in UPEC isolates, followed by aac3-II (80.4%) among the five genes tested, blaTEM, aac3-II, sul2, hlyA, and fimH. The correlation between antibiotic resistant patterns and the presence aac3-II gene was significantly high. The resistance to the sulfonamides’ combined antibiotic was highly correlated with the presence of sulf2 gene. Conclusion: Antimicrobial resistance was significantly linked to phenotypic and genotypic virulence factors. These results will aid in elucidating the pathogenicity of UTIs and guiding treatment decisions. Keywords: UPEC resistance profile; virulence factor; Biofilm formation; hemagglutinin; hemolysin.