This review summarizes recent work examining the interaction between host and parasite in recurrent
urinary tract infection (UTI) and renal
scarring. Virulence in uropathogenic E. coli has been defined by the severity of
acute disease. Isolates from patients with acute pyelonephritic strains differ from those causing asymptomatic
bacteriuria by multiple traits which contribute to virulence, and which are coexpressed in a non-random manner. The single marker most characteristic for the pyelonephritogenic clones is bacterial adherence to uroepithelial cells binding specifically to the disaccaride
Gal alpha 1-4 Gal beta within the globoseries of
glycolipids. The notion that the most severe consequence of acute
pyelonephritis, i.e. renal
scarring, was caused by the most virulent clones, was contradicted by comparison of pyelonephritic strains isolated from children with and without
scarring. The virulent clones were significantly less frequent in patients with renal
scarring (22%) than in patients with recurrent
pyelonephritis not developing renal
scars (62%). In view of the unexpected inverse association of bacterial virulence with renal
scarring lack of
Gal alpha 1-4 Gal beta binding capacity of E. coli strains was found to predict the risk for renal
scarring among boys with first-time acute
pyelonephritis. Vesicoureteric reflux (VUR) is widely accepted as a host determinant of susceptibility to
pyelonephritis and renal
scarring. In our study the frequency of renal
scarring was 57% among girls with VUR as compared to 8% of those without. The reflux alone did however, not explain the selection of bacteria of low virulence. Individuals prone to UTI and renal
scarring were found to be a genetically selected subgroup of the general population. A correlation between P1
blood group phenotype and susceptibility to UTI and between
blood group non-secretor state and renal
scarring was found. The mechanisms behind these relationships need to be defined. The bacterial and host parameters combined indicate that host parameters are essential for the tendency to develop renal
scarring after acute
pyelonephritis.