The third lecture, entitled "The urogenital barrier, from acute rupture to chronic parasitism", reviewed the anatomo-histology of the urogenital tract in order to define the potential strengths and weaknesses of this barrier with regard to the colonization and invasion of the urinary tract by pathogenic bacteria. Uropathogenic Escherichia coli (UPEC), the most common etiological agent of urinary tract infections, was used as a model. The "panoply" of genes and pathogenicity islands underlying the UPEC pathovar was considered, with particular emphasis on the differentiation between strains responsible for chronic/recurrent infections of the lower urinary tract (cystitis) and those responsible for pyelonephritis. The pathophysiology of these two types of infection was reviewed in detail. In the case of bladder infection, recent data such as the internalization and formation of "intracellular biofilms" by strains expressing type 1 pili were detailed, as they target very long-lived epithelial cells (6 months): this could explain recurrence and chronicity, without the need, in women, to consider regular reseeding from the intestinal flora. This hypothesis would considerably modify prevention schemes.
With regard to infection of the upper urinary tract, the pathophysiological basis of pyelonephritis was detailed, with particular emphasis on the type of bacterial adhesion factors required (Pap pili adhering to di-galactoside residues on epithelial cells) and on new developments concerning the pathophysiology of infection of the renal parenchyma once the tubular barrier has been breached. The role of anoxia and coagulation in the development and local control of pathogen dissemination was developed. Finally, emphasis was placed on the current uncertainties concerning the understanding of retrograde progression of UPEC in the ureter in the absence of reflux.
