Investigation of virulence genes of escherichia coli strains isolated from bacteremic and non-bacteremic patient samples prediagnosed as urinary system infections

Escherichia coli, which is the most common cause of urinary system infections, is also one of the most common infectious agents causing sepsis. E. coli septicemia may occur after digestive system perforation, appendicitis or surgical intervention, as well as spread to the blood during urinary tract infections. Factors that determine the pathogenesis of E. coli for a system or tissue are some virulence factors and therefore genes that encoding these factors. Virulence factors of E. coli include adhesins, toxins, invasins, capsules, movement, outer membrane proteins, serum resistance, siderophores and biofilm formation abilities. Contribution to bacteriemia of these virulence factors has not been fully explained. For this reason, this study aimed to determine the presence of some virulence genes in E. coli isolates causing nonbacteremic urinary system infections (NBUSI) and bacteremic urinary system infections (BUSI). 50 E. coli isolates causing NBUSI and 50 causing BUSI were included in the study. The presence of 19 virulence genes or alleles (sfaS, kpsMTII K1, cnf1, sfa/focDE, papEF, ibeA, hlyA, kpsMTII, cdtB, focG PapGII, ompT, hlyD, cdt1, papA, papA allel F7-2, papA allel F8, papA allel F10 ve papA allel F16) that were reported to contribute to bacteriemia in different studies according to literature survey was investigated by polymerase chain reaction (PCR). In addition, the presence of the chuA, yjaA genes and TSPE4.C2 DNA fragment in the isolates was investigated by the same method and phylogenetic groups of the isolates were determined by evaluating the results with a dichotomous decision tree. Antibiotic susceptibilities of isolates was determined by Kirby-Bauer disc diffusion method. ESBL presence was determined by combination disc diffusion test. As a result, papA, papGII, papEF, hlyA, hlyD and cnf1 genes were found to be significantly higher in strains causing BUSI than strains causing NBUSI. papA, papA allel F10, papGII, papEF, sfa/focDE, sfaS, focG, hlyA, hlyD, kpsMTII, kpsMTII K1, ibeA, cnf1 ve ompT genes were significantly more abundant in the B2 phylogenetic group than in the non-B2 phylogenetic groups. cdtB gene was significantly more abundant in the B1 phylogenetic group than in the non-B1 phylogenetic groups. papA allel F10 gene was significantly more abundant among ampicillin (AM), amoxicillin-clavulanic acid (AMC), piperacillin-tazobactam (TZP), Cefuroxime axetil (CXA), cefixime (CFM), cefotaxim (CTX), ceftriaxone (CRO), ceftazidime (CAZ), cefepime (FEP), ciprofloxacin (CIP) and levofloxacin (LEV) resistant strains than susceptible strains. papEF gene was significantly more abundant among CIP and LEV susceptible strains than resistant strains. Sfa/focDE gene was significantly more abundant among AM, AMC, CXA, CFM, CTX, CRO, CAZ, FEP, CIP, LEV and trimethoprim sulfamethoxazole (SXT) susceptible strains than resistant strains. sfaS gene was significantly more abundant among AMC susceptible strains than resistant strains. focG gene was significantly more abundant among AM, AMC, FEP, CIP, LEV and SXT susceptible strains than resistant strains. kpsMTII gene was significantly more abundant among SXT susceptible strains than resistant strains. kpsMTII K1 gene was significantly more abundant among AM, AMC, CXA, CFM, CTX, CRO, CAZ, FEP, gentamicin (CN), CIP, LEV and SXT susceptible strains than resistant strains. papA allel F10 gene was found to be significantly higher in strains isolated from male patients than strains isolated from female patients. KpsMTII K1 gene was found to be significantly higher in strains isolated from patients aged ≤ 50 years than strains isolated from patients aged > 50 years. As a result, papA, papGII, papEF, hlyA, hlyD and cnf1 genes were found higher in strains causing BUSI. This study shows that, none of these genes can become biomarkers on its own at showing an isolate of E. coli can cause bacteriemia, but presence of some genes may indicate increases the probability of developing bacteraemia. Furthermore, it is thought that expression levels of the genes may have more importance than their existance.