Abstract
An experimental pyelonephritis model was developed in monkeys (Macaca fascicularis) using P-fimbriated Escherichia coli as the infecting organism. The relevant receptor molecules for P-fimbriae were also shown to be present in Macaca fascicularis. Atraumatic administration of P-fimbriated E. coli into the ureter induced a ureteritis followed by acute and chronic pyelonephritis. The decisive role of P-fimbriae as an adhesive virulence factor was proven by the receptor blockade of P-fimbriae-mediated bacterial adhesion by a synthetic receptor analogue (alpha-D-Galp-(1-4)-beta-D-Galp-1-OMe), which was administered into the ureter together with the challenge bacteria. On the basis of these and other findings, the role of reflux and pyelonephritis in relation to renal scarring is discussed in this paper. It is proposed that minor transitional vesicoureteral reflux together with the adhesive property of P-fimbriated E. coli and their ability to induce ureteritis might constitute an alternative mechanism to gross reflux by which bacteria ascend to the kidney. These findings and the fact that intestinal colonization with P-fimbriated E. coli coincides with the disease have opened up new prophylactic and therapeutic possibilities.
Published Version
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