In the neonatal period, UTI originates via hematogenous spread resulting in bacterial seeding of the renal parenchyma. After the neonatal period, bacteria gain access to the urinary tract via perineal and periurethral colonization, with subsequent retrograde contamination of the lower urinary tract structures. Virulence of the pathogen, host immunity, and structural and functional aspects of the urinary tract all play important roles in the development of UTI. Much is known about structural and functional factors contributing to the risk of UTI. Congenital urinary tract anomalies, vesicoureteral reflux, and urolithiasis are associated with a higher incidence of UTI.3,45 and 6 However, it is now clear that pyelonephritis in the absence of vesicoureteral reflux is far more common than previously thought. Behavioral and functional factors, such as poor hygiene, voluntary urinary retention, and constipation, have been associated with increased risk of UTI. 78

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