Recent discoveries have added to our understanding of how bacterial virulence factors and host defense mechanisms interact to produce the varied syndromes of urinary tract infection. P fimbriae have retained their pre-eminence among the urovirulence factors of Escherichia coli, but new data challenge several accepted notions regarding this adhesin. Iatrogenic alterations in the vaginal flora can either increase or decrease the risk of recurrent urinary tract infection. Person-to-person transmission of uropathogenic strains and self-reinfection probably occur more commonly than previously recognized. Organisms of low intrinsic virulence can cause serious urinary tract infection in compromised hosts, and seemingly mild infection episodes may be associated with bacteremia and renal failure in selected patients. Locally produced interleukin-8 may be the main chemoattractant cytokine responsible for pyuria during urinary tract infection. The roles of cell-mediated and humoral immunity in defense against urinary tract infection remain controversial.