Urinary Tract Infection: How It Happens?

Urinary tract infections (UTIs), including cystitis and pyelonephritis, affect a large proportion of the  world population and account for substantial morbidity and medical costs. Classification of the UTIs is based on the anatomical level of infection, the grade of severity of infection, the underlying risk factors,  and the microbiological findings. Uropathogenic Escherichia coli is the causative agent in 70-95% of  community-acquired uroinfections and about 50% of all cases of nosocomial uroinfections. Virulence  factors associated with uropathogenic strains of E. coli contain toxins such as haemolysin and cytotoxic  necrotising factor, capsules, lipopolysaccharide, the siderophore aerobactin, and adhesive organelles. The  ability to attach to urothelial cells is the most important determinant of pathogenicity. An adherence is  followed by inflammation involving the urothelial cells’ cytokine response. Whereas interleukin (IL)-6 can cause the fever and systemic response of the UTIs, IL-8 can function as a neutrophil chemoattractant.  Cytokines released by T cells and monocytes modify initiative urothelial cells’ cytokine response to  bacteria. Nevertheless, antibiotic treatments can effectively sterilise the urine, but bacteria can survive and  persist in the bladder tissue, serving as a reservoir for the recurrent UTIs. The severity of UTI reflects the  quality and magnitude of the host response. While strong local and systemic innate immune activation  occurs in patients with acute pyelonephritis, the response to asymptomatic bacteriuria is low. It should be reasonable to ‘individualise’ diagnosis and therapy by interconnecting information on uropathogenic bacterial virulence and the host response.