@article{HackerHughesHofetal.1983,
  author    = {Hacker, J{\"o}rg and Hughes, C. and Hof, H. and Goebel, W.},
  title     = {Cloned hemolysin genes from Escherichia coli that cause urinary tract infection determine different levels of toxicity in mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59330},
  year      = {1983},
  abstract  = {After intraperitoneal injection of mice with Escherichia coli strains isolated from patients with urinary tract infections, the mortality due to hemolytic (Hly+) and nonhemolytic (Hiy-) isolates was 77 and 40\%, respectively. Deletion of the chromosomal hemolysin (h/y) determinant in an E. co/i 06:K15:H31 urinary tract infection strain led to a significant reduction in toxicity for mice, and its reintroduction on a recombinant plasmid partially restored the original toxicity. Although introduction of the cloned plasmid pHiy152-encoded hly determinant into the Hly- E. coli 06 mutant strain increased toxicity by only a marginal degree, transformation with the cloned chromosomal hly determinants from two E. coli strains of serotypes 018ac:K5:H- and 075:K95:H? resulted in markedly greater toxicity, even exceeding that of the original Hly+ E. coli 06 wild-type strain.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HackerOttHof1993,
  author    = {Hacker, J{\"o}rg and Ott, M. and Hof, H.},
  title     = {Effects of low, subinhibitory concentrations of antibiotics on expression of a virulence gene cluster of pathogenic E. coli by using a wild-type gene fusion},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59874},
  year      = {1993},
  abstract  = {No abstract available},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HackerHofEmoedyetal.1986,
  author    = {Hacker, J{\"o}rg and Hof, H. and Em{\"o}dy, L. and Goebel, W.},
  title     = {Influence of cloned Escherichia coli hemolysin genes, S fimbriae and serum resistance on pathogenicity in different animal models},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59423},
  year      = {1986},
  abstract  = {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.},
  subject      = {Infektionsbiologie},
  language  = {en}
}