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Since the introduction of routine immunization against Haemophilus influenzae type b and Streptococcus pneumoniae, urinary tract infections (UTIs) have replaced bacteremia and meningitis as the most common serious bacterial infection in children. Identification and treatment of UTIs are important in managing signs and symptoms such as fever and dysuria, and also for preventing and minimizing the morbidity associated with pyelonephritis and sepsis. The site of infection may be the bladder (cystitis), ureters (ureteritis), pelvis (pyelitis), and/or renal parenchyma (pyelonephritis).


The pathogenesis of UTI depends on a complex interaction between bacterial and host factors. The urinary tract is normally a sterile environment with nearby bacterial reservoirs in the distal urethra, periurethral region, perianal region, perineum, and vagina. With normal hydration and spontaneous voiding, the urinary flow through the distal urethra helps to prevent bacterial ascension into the bladder. Maintenance of normal flora prevents more virulent strains from colonizing the gut and the periurethral area; an individual’s microbiome may be influenced by age, hormones, recent antibiotic use, hygiene, or spermicides.

The majority of UTIs are initiated by bacteria that ascend the urethra and adhere to the mucosal lining of the bladder; a hematogenous source that seeds the urinary tract is much less common but is also possible. The most studied model of bacterial adhesion in the urinary tract is the “P” fimbriae expressed on the surface of uropathogenic Escherichia coli. These bacterial proteins enable adherence of uropathogenic E coli to the bladder. They are referred to as P fimbriae because they can recognize and agglutinate erythrocytes of the P1 blood group. The P blood group antigen is also present on human uroepithelial cells.

Following adhesion, the bacteria may invade across the mucosal barrier and trigger an inflammatory host reaction. White blood cells (WBCs) are then recruited to respond to the bacterial invasion, resulting in leukocytes appearing in the urine (pyuria). The inflammatory response results in the typical symptoms of cystitis including dysuria, urinary frequency, and urgency.

Understanding the pathogenesis of UTI clarifies how certain factors can increase the risk of UTI. For example, bacterial ascension via adherence to the urethra and bladder may be facilitated by infrequent or dysfunctional voiding. Dysfunctional voiding refers to the lack of coordination between 2 processes that are essential for normal voiding to occur—relaxation of the urethral sphincter and contraction of the detrusor muscle of the bladder. The failure of the voluntary sphincter to relax causes an obstruction to the urine outflow during voiding. Coordinated bladder-sphincter control and efficient elimination of urine with a brisk urine outflow across the urethra is a natural defense mechanism against bacterial ascension and adherence. Toilet training is a period during which the risk for UTI rises as the child may inappropriately tighten and relax the sphincter to be socially continent. Children being evaluated for recurrent UTIs will often exhibit dysfunctional ...

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