Influence of cloned Escherichia coli hemolysin genes, S-fimbriae and serum resistance on pathogenicity in different animal models

Abstract

The virulence of the uropathogenic E. coli strain 536 (06:K15:H31) which produces the S-fimbrial adhesin (Sfa +), is serum-resistant (Sre +) and hemolytic (Hly +) and its derivatives were assessed in five different animal models. Cloned hemolysin ( hly) determinants from the chromosomes of 06, 018 and 075 E. coli strains and from the plasmid pHly 1 52 were introduced into the spontaneous Sfa −, Sre −, Hly − mutant 536-21 and its Sfa +, Sre +, Hly − variant 536-31. As already demonstrated for the 536-21 strains ( Infect. Immun. 42: 57–63) the 018- hly determinant but not the plasmid-encoded hly determinant of pHly152 transformed into 536-31 contribute to lethality in a mouse peritonitis model. Similar results were obtained with both Hly − host strains and their Hly + transformants in a chicken embryo test and in a mouse nephropathogenicity assay in which the renal bacterial counts were measured 15 min to 8 hours after i.v. infection. S-fimbriae and serum resistance had only a marginal influence in these three in vivo systems. In contrast all three factors, S-fimbriae, serum resistance and hemolysin, were necessary for full virulence in a respiratory mouse infection assay. In a subcutaneously-induced sepsis model in the mouse restoration of S-fimbriae and serum resistance and separately chromosomally-encoded hemolysis increased virulence to a level comparable to that of the parental 536 strain.