**1. Introduction**

Urinary tract infections (UTIs) are an important medical problem, being the second most common bacterial infection of humans after respiratory tract infection. They are often recurrent,

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frequently difficult to treat, and can cause parenchymal damage to the kidney, leading to renal insufficiency and further complications [1–3]. UTIs impose a substantial burden on society and the health care system in relation to diagnosis, management, lost productivity, morbidity, and sometimes death [4–6]. Furthermore, increasing resistance to therapeutically important antimicrobial agents and the recent emergence of the virulent and multidrug-resistant ST131 clonal group have made UTI management progressively more costly and challenging [7, 8]. Several studies suggest that a greater array of VFs is generally needed to cause more invasive UTIs, although the extent appears to differ according to age and gender. Thus, further studies targeting VFs, which have been proposed as the best target for vaccine development, are needed. A better understanding of UTI pathogenesis, especially for the most common cause of UTI, namely *Escherichia coli*, is crucial for treatment and prevention of UTIs.

Among bacterial infections in children, UTI ranks highly, even outnumbering bacterial meningitis, pneumonia, and bacteremia [15]. About 1% of infants < 3 months old develop UTI, with more males affected than females. Proper and urgent UTI management is crucial in children as an estimated 10–15% of children with UTI will develop permanent kidney damage, leading to

The Pathogenesis of *Escherichia Coli* Urinary Tract Infection

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The propensity of UTIs to recur, often within a few weeks or months after an initial acute infection, is a problem in UTI management. Approximately 20–30% of women will have a recurrent bladder infection within 6 months after an initial episode, and an additional 3% will

UTI pathogenesis is a complex process that is influenced by various host biological and behavioral factors, and by properties of the infecting pathogen, including VFs. This presents a challenge in epidemiological studies regarding the role of specific VFs in UTI pathogenesis

In most noncompromised individuals, the urinary tract is normally sterile, and the entry of exogenous microorganisms is prevented by urine flow, secreted and tissue-associated antibacterial factors, and the bactericidal activities of effector immune cells. In most cases, the host fecal flora is the source of the infecting *E. coli* strain, and spreads via the perineal, vaginal, and periurethral areas to the lower urinary tract (i.e., urethra and bladder) where they may establish colonization [20]. Two hypotheses have been proposed to explain the movement of the organism from the fecal flora to the urinary tract. The prevalence hypothesis holds that the numerically most prevalent *E. coli* clones in the feces will be involved, whilst the pathogenicity theory holds that *E. coli* strains with enhanced virulence potential will be selected [20]. These two mechanisms may not be mutually exclusive, but instead may jointly contribute to UTI

Although the host's fecal flora is the major source of the *E. coli* infecting strain, other proximal external reservoirs of the organism have been described. Community outbreaks of UTI have been reported [22–24], but without any evidence of person-to-person transmission. Foods and water have been proposed as possible vehicles of such outbreaks [22–24]. Specifically, extensive molecular similarities between *E. coli* from retail meat products and healthy or infected humans have been described [22]. Within-household spread of *E. coli* among co-habitating humans and their pets, including between sexual partners, have been confirmed [4, 10, 11]. The VFs of the invading bacteria and the host's defense mechanisms determine the outcome of the infection [25]. A variety of host factors, such as age, gender, pregnancy, or immunological status, may predispose to UTI and allow less virulent pathogens to cause the disease [20]. If the infection is confined to the lower urinary tract, with symptoms such as dysuria and frequency of urination, the infection is referred to as acute cystitis. If the infection spreads to the upper urinary tract with symptoms such as flank pain, fever, and malaise, the infection is

other chronic diseases such as hypertension and renal insufficiency [16, 17].

experience a third infection [18, 19].

**4.** *E. coli* **UTI pathogenesis**

pathogenesis [21].

defined as an acute pyelonephritis.

because of the confounding effect of host factors.
