THE PAPG-ADHESIN AT THE TIP OF P-FIMBRIAE PROVIDES ESCHERICHIA-COLI WITH A COMPETITIVE EDGE IN EXPERIMENTAL BLADDER INFECTIONS OF CYNOMOLGUS MONKEYS

Human urinary tract infection is an infectious disease that depends on a series of host-microbial interactions. The bacteria first colonize the colon and then the periurethral/vagnal areas; they ascend to and i nfect first the bladder and then the kidneys. Expression of Escherichi a coli P-fimbriae constitutes the strongest correlation to renal patho genicity, but is also related to first-time cystitis in children. The role of P-fimbriae in the preceding steps in the infectious process is unknown. To examine this, we constructed, from a P-fimbriated E. coli strain with a class II G-adhesin preferentially binding to globoside, one isogenic mutant lacking the G-adhesin and another isogenic mutant in which we replaced the papG class II allele with a class III adhesi n preferentially binding to the Forssman antigen. We report here the c omparison oi the adhesin knockout mutant (DS17-8) and the class-switch mutant (DS17-1) with the wild-type (DS17) for in vivo colonization of the gut, vagina, and bladder of cynomolgus monkeys. It was recently s hown that the class II tip G-adhesin is a prerequisite for acute pyelo nephritis to occur in the monkey model in the absence of other kidney- specific adhesins or obstruction of the urinary now. Here we show that it is not required for bladder infection but gives a competitive adva ntage in mixed infections. In the vagina and colon, the G-adhesin give s no competitive advantage.