Urinary tract infections (UTls) have traditionally been viewed as acute and
often self-limiting infections caused predominantly by noninvasive Escheri
chia coli, However, this concept has been challenged by recent findings dem
onstrating that an acute bladder infection results from a complex series of
host-pathogen interactions that can lead to bacterial invasion and persist
ence and that ultimately can determine the course of the infectious disease
. The ability of E. coli to gain a foothold in the bladder is greatly facil
itated by type pilus-mediated attachment to and invasion of bladder epithel
ial cells. Invasion allows uropathogenic strains of E. coli to exploit the
intracellular environment by replicating within these epithelial cells whil
e evading a multitude of host defenses. An intracellular location also prov
ides them a safe haven from many common antibiotic therapies. However, atta
chment and invasion also activates a cascade of innate host defenses, leadi
ng to the death and exfoliation of bladder cells and the production of infl
ammatory mediators. The ability of uropathogenic E. coli to flux out of cel
ls and colonize surrounding cells provides them a mechanism to subvert thes
e defense mechanisms and persist in the bladder epithelium for weeks follow
ing the acute infection. The persistence of E. coli in bladder tissue may b
e relevant to more chronic diseases of the urinary tract such as recurrent
UTls and interstitial cystitis. (C) 2001, Elsevier Science Inc.