BACTERIAL ADHERENCE AS A VIRULENCE FACTOR IN URINARY-TRACT INFECTION

Escherichia coli (E. coli) causes > 90% of urinary tract infections, UTI, in childhood. The capacity to adhere to urinary tract epithelial cells characterizes E. coli strains that cause acute pyelonephritis. Adherence of uropathogenic E. coli is the result of a specific interaction between bacterial adhesins and glycolipid receptors on the host cells, especially the globoseries of glycolipids which share the Galactose-alpha-1- > 4Galactose-beta-disaccharide (Gal-alpha-1- > 4Gal-beta). In childhood UTI, Gal-alpha-1-4Gal-beta-binding bacteria caused significantly higher body temperature, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and pyuria, and lower renal concentrating capacity, than E. coli lacking this specificity. The Gal-alpha-1- >4Gal-beta-binding bacteria thus appeared to be more potent inducers of inflammation than other strains. Since inflammation may lead to tissue damage we examined the relationship of infection with Gal-alpha-1- >4Gal-beta-positive bacteria to renal scarring. The frequency of renal scarring was 5% in boys with Gal-alpha-1- >4Gal-beta-positive and 40% in boys with Gal-alpha-1- >4Gal-beta-negative E. coli. Bacterial binding to Gal-alpha-1- >4Gal-beta can be detected with a commercially available test reagent. This reagent can thus be used as an effective predictor of risk for renal scarring. Interleukin-6 (IL-6) is a pyrogen and inducer of the acute phase reactants. It was shown to be produced locally in the urinary tract, in response to UTI, and to spread systemically. Mucosal challenge with dead bacteria was sufficient to induce the IL-6 response. Circulating IL-6, and/or IL-1 and tumor necrosis factor could explain the fever, as well as increased ESR and CRP found in association with acute symptomatic UTI.