The Pathogenesis of Urinary Tract Infections

Urinary tract infections (UTIs) are among the most common conditions requiring medical treatment with 6-10% of all young females demonstrating bacteriuria (Raz 2001). The incidence of UTIs increases with age and 25-50% of females aged 80 or more have bacteriuria (Abrutyn et al. 1988). UTIs occur as a result of interactions between the uropathogen and host and their pathogenesis involves several processes. Initially the uropathogen attaches to the epithelial surface; it subsequently colonises and disseminates throughout the mucosa causing tissue damage. After the initial colonisation period, pathogens can ascend into the urinary bladder resulting in symptomatic or asymptomatic bacteriuria. Further progression may lead to pyelonephritis and renal impairment. Specific virulence factors residing on the uropathogen’s membrane are responsible for bacterial resistance to the normally effective defence mechanisms of the host. Recently, bacterial adhesins and their associated epithelial binding sites have been identified and natural antiadherence mechanisms are currently under investigation. An understanding of pathogenic and anti-adherence mechanisms may allow physicians to develop appropriate strategies for UTI prevention and adequate management protocols. In the present chapter we discuss current concepts on the pathogenesis of UTIs with particular emphasis on pathogenic bacteria, virulence factors, predisposing factors, natural defences within genitourinary tract and consequences when these defence mechanisms are altered.