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

Abstract

of cloned hemolysin genes, S-fimbriae and serum resistance on pathogenicity in different animal models. Microbial Pathogenesis 1986; 1: 000-000.The virulence of the uropathogenic E. coli strain 536 (06: K 1 5: H31) which produces the S-fimbrial adhesin (Sfa•), is serum-resistant (Sre+) and hemolytic (Hiy+) and its derivatives were assessed in five different animal models. Cloned hemolysin (h/y) determinants from the Chromosomes of 06,018 and 075 E. colistrains and from the plasmid pHiy152 were introduced into the spontaneaus Sfa-, Sre-, Hly-mutant 536-21 and its Sfa+, Sre+, Hly-variant 536-31. As already demonstrated for the 536-21 strains {lnfect. Immun. 42: 57-63) the 018-hly determinant but not the plasmid-encoded hly determinant of pHiy 1 52 transformed into 536-31 contribute to lethality in a mouse peritonitis modal. Similar results were obtained with both Hlyhost strains and their Hly+ transformants in a chicken embryo test and in a mouse nephropathogenicity assay in which the renal bacterial counts were measured 1 5 min to 8 hours after i.v. infection. S-fimbriae and serum resistance had only a marginal influence in these three in vivo systems. ln centrast all three factors, S-fimbriae, serum resistance and hemolysin, were necessary for full virulence in a respiratory mouse infection assay. ln a subcutaneously-induced sepsis model in the mouse restoration of S-fimbriae and serum resistance and separately chromosomally-encoded hemolysis increased virulence to a Ievel comparable to that of the parental 536 strain.Key words: E. coli hemolysin. S-fimbriae; serum resistance. E. coli virulence; animal models; gene cloning. lntroductionEscherichia coli strains are responsible for most urinary tract infections (UTI). Certain E. coli clones cause neonatal sepsis and meningitis. 1 -3 Many cell components such as adhesins, serum resistance factors, cytolysins and others have been shown to be associated with extraintestinal virulence in E. coli. 4 Adhesion factors which recognize galactosyl-galactose receptors (P fimbriae 2 · 5 ) are common among UTI strains. S-fimbriae specifically bind to sialic acid containing structures are frequently associated with isolates from cases of newborn meningitis.3·6 The genetic determinants for S~fimbrial adhesins (sfa) cover a stretch of

Virulence factors in Escherichia coli urinary tract infection

“…Animal Studies Hemolytic strains are more lethal than nonhemolytic strains for chicken embryos (116,173,206,275,353) and for mice or rats in models of peritonitis (116,173,175,198,275,500,603,604), respiratory infection (115,173), and hematogenous pyelonephritis (136,137,173,310,565,566,587,589,590), causing hemorrhagic lung lesions and hemoglobinuria in mice in addition to increased mortality (116,500). In mouse and rat models of ascending UTI, hemolysin production is associated with increased bladder colonization and nephropathogenicity (97,212,265,340).…”

Molecular Analysis of Bacterial Cytolysins

“…Type I mutants are nonvirulent when tested in several animal models [10] and thus can be used as suitable hosts for reconstitution of virulence by reintroduction of cloned virulence genes. Hemolysin determinants from various origins were introduced with and without the sja genes in such mutants.…”

Virulence Genes and Antimicrobial Susceptibilities of Hemolytic and Nonhemolytic Escherichia coli Isolated from Post-Weaning Piglets in Central Thailand

“…Besides these toxins, the -hemolytic property is thought to be an important virulence factor in pathogenic strains of E. coli [16]. In extraintestinal infections, hemolysin is a component necessary for complete virulence in pneumonic lesions in a rat model and increases sepsis of subcutaneous healing in a mouse model [17].…”