## 1 Introduction  
Uriany tract infections (UTIs) are among the most frequently occurring major bacterial infections worldwide, and their significant increase in incidence in recent years is alarming [1; 2; 3]. It is estimated that 150 million UTIs occur annually worldwide, with significant morbidity and high treatment costs affecting the efficiency of national health care systems [4]. In the US alone, each year, more than 10 million doctor office visits, 2 million emergency department visits, and 100,000 hospitalizations are associated with UTIs [5; 6]. Those at high risk are newborns, pre-school girls, sexually active women, and older people of both sexes [7]. UTIs mainly affect the female population, which is related to the structure of the urinary tract. A cohort study among 2000 women representing the US population corroborates this finding [8; 9]. The prevalence of UTIs results in rampant use of antibiotics, which impacts the spread of resistance. This is a clinical problem, especially in recurrent UTIs [10]. Therefore, empirical treatment of emergency room patients is a challenge for clinical urology and requires the constant evaluation of bacterial susceptibility to antibioticsUTIs have been associated with such bacterial species as Pseudomonas aeruginosa, Acineobacter baumannii, Staphylococcus aureus, and those belonging to the Enterobacteriaceae family, such as Klebsiella pneumoniae, Proteus mirablis, Citrobacter, and Enterobacter, as well as some Candida species [11; 12]. However, uropathogenic Escherichia coli (UPEC) are most commonly responsible for about 80% of uncomplicated UTIs, 95% of out-of-hospital infections, and 50% of hospital-acquired infections [13]. UPEC are included in the ExPEC pathotype, along with other E. coli isolates involved in various extraintestinal infections. UPEC strains have evolutionarily adapted to colonize a niche in the urinary tract. They harbor genetic virulence factors (VF) on pathogenicity-associated islands (PAIs) [14], contributing to bacterial pathogenesis and distinguishing them from commensal strains [15]. Phylogenetic analyses have shown that E. coli strains classify into four major phylogenetic groups (A, B1, B2, and D), of which those belonging to groups B2 or D are most often responsible for extraintestinal infections [16]. Eight phylogenetic groups are currently recognized by the classification established by [PERSON]: seven (A, B1, B2, C, D, E, F) belong to E. coli sensu stricte, while a distinct example is Escherichia cryptic clade I [17]. UPEC virulence requires coordinated expression of multiple genes that facilitate adhesion and colonization in the urinary tract. One can distinguish between VFs bound to the bacterial cell surface and those that are secreted and exported to the site of action. Adhesion to tissues within the urinary tract is the most important step in pathogenicity and is enabled by adhesion factors. These include various types of fimbiae (types 1, P, S, F1C), fimbrial Dr adhesins, as well as afimbrial Afa adhesins and PapC. Among the toxins that help bacteria spread to deeper tissues after disrupting cell integrity and that can cause an inflammatory response, the most important are the lipoproteins--\(\alpha\)-hemolysin (HlyA) and cytotoxic necrosis factor 1 (CNF1) [18; 19]. Moreover, the main component of the cell wall--lipopolysaccharide (LPS), antigen O and K--is an endotoxin that helps suppress the host immune system [20]. The availability of iron is very limited in the urinary tract, so in order to survive in this environment, bacteria encode proteins of iron-acquiring systems. UPEC strains are particularly well-equipped with the factors required for biosynthesis and uptake of the following siderophores: enterobactin, aerobactin, yersiniabactin and salmonchin, which they then transport into their cytoplasm through the Sit system (siderophore-iron transporter proteins, SitABCD) [21].