Contribution of cloned virulence factors from uropathogenic Escherichia coli strains to nephropathogenicity in an experimental rat pyelonephritis model.
Escherichia coli 536 (O6:K15:H31), which was isolated from a case of urinary tract infection, determines high nephropathogenicity in a rat pyelonephritis system as measured by renal bacterial counts 7 days after infection. The loss of S fimbrial adhesin formation (Sfa-) (mannose-resistant hemagglutination [Mrh-] and fimbria production [Fim-]), serum resistance (Sre-), and hemolysin production (Hly-) in the mutant 536-21 led to a dramatic reduction of bacterial counts from almost 10(5) to only 40 cells per g of kidney. The reintroduction of the cloned S fimbrial adhesin determinant (sfa) increases the virulence of the avirulent mutant strain by a factor of 20; almost the same effect was observed after restoration of serum resistance by integration of an sfa+ recombinant cosmid into the chromosome. Additional reintroduction of the Hly+ phenotype by transformation of two hly determinants increased the virulence of the strains. Hemolysin production determined increased renal elimination of leukocytes and erythrocytes. Thus all three determinants investigated, S fimbriae, serum resistance, and hemolysin, contribute to the multifactorial phenomenon of E. coli nephropathogenicity.
D018830:Adhesins, Escherichia coli; D000818:Animals; D001422:Bacterial Adhesion; D001426:Bacterial Proteins / Q000235:genetics; D001770:Blood Bactericidal Activity; D003001:Cloning, Molecular; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity*; D010861:Fimbriae, Bacterial; D006388:Hemagglutinins / Q000235:genetics*; D006460:Hemolysin Proteins / Q000235:genetics*; D011704:Pyelonephritis / Q000382:microbiology*; D051381:Rats
D018830:Adhesins, Escherichia coli; D001426:Bacterial Proteins; D006388:Hemagglutinins; D006460:Hemolysin Proteins