@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{HackerSchmidtHughesetal.1985,
  author    = {Hacker, J{\"o}rg and Schmidt, G. and Hughes, C. and Knapp, S. and Marget, M. and Goebel, W.},
  title     = {Cloning and characterization of genes involved in the production of mannose-resistant, neuraminidase-susceptible (X) fimbriae from an uropathogenic O6:K15:K31 Escherichia coli strain},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59353},
  year      = {1985},
  abstract  = {The Qropathogenic Escherichia coli strain 536 (06:K15:H31) exhibits a mannose-resistant hemagglutination phenotype (Mrh) with bovine erythrocytes and delayed Mrh with human and guinea pig erythrocytes. Neuraminidase treatment of the erythrocytes abolishes mannose resistant hemagglutination, which is typical for X fimbriae. E. coli strain 536 synthesizes two different fimbriae (Fim phenotype) prQtein subunits, 16.5 and 22 kilodaltons in size. In addition the strain shows mannose-sensitive hemagglutination and common type I (Fl) fimbriae. The cosmid clone E. coli K-12(pANN801) and another nine independently isolated Mrh+ cosmid clones derived from a cosmid gene bank of strain 536 express the 16.5-kilodalton protein band, bot not the 22-kilodalton protein, indicating an association of the Mrh+ property with the "16.5-kilodalton fimbriae." All cosmid clones were fimbriated, and they reacted with antiserum produced against Mrh+ fimbriae of the E. coli strain HB101(pANN801) and lacked mannose-sensitive hemagglutination (Fl) funbriae. From the Mrh fim cosmid DNA pANN801, several subclones coding for hemagglutination and X fimbriae were constructed. Subclones that express both hemagglutination and fimbriae and subclones that only code for the hemagglutination antigen were isolated; subclones that only produce fimbriae were not detected. By transposon Tn5 mutagenesis we demonstrated that about 6.5 kilobases of DNA is required for the Mrh+ Fim+ phenotype, and the 1.5- to 2-kilobase DNA region coding for the structural proteiil of the fimbriae has been mapped adjacent to the region responsible for the Mrh+ phenotype. Two different regions can thus be distinguished in the adhesion determinant, one coding for hemagglutination and the other coding for fimbria formation. Transformation of plasmid DNA from these subclones into a Mrh- Fim- mutant of E. coli 536 and into a galE (rough) strain of Salmonella typhimurium yielded transformants that expressed both hemagglutination and fimbria production.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HughesHackerDueveletal.1987,
  author    = {Hughes, C. and Hacker, J{\"o}rg and D{\"u}vel, H. and Goebel, W},
  title     = {Chromosomal deletions and rearrangements cause coordinate loss of hemolysis, fimbriation and serum resistance in an uropathogenic strain of Escherichia coli},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59470},
  year      = {1987},
  abstract  = {No abstract available},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HughesHackerRobertsetal.1983,
  author    = {Hughes, C. and Hacker, J{\"o}rg and Roberts, A. and Goebel, W},
  title     = {Hemolysin production as a virulence marker in symptomatic and asymptomatic urinary tract infections caused by Escherichia coli},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59346},
  year      = {1983},
  abstract  = {Potential virulence, as defined by combined Ievels of adhesion to urinary epithelial cells, serum resistance, and mouse toxicity, was assessed for Escherichia coli strains causing symptomatic and asymptomatic urinary tract infections in relation to the carriage of hemolysin and other suspected virulence determinants. Hemolysin production (Hly), associated with certain 0 (04, 06, 018, and 075), K (5), and hemagglutination (VI and VII) antigenic types but not colicin V production (Cva), was evident in 83 and 60\% ofisolates in groups possessing high potential virulence andin only 11 and 6\% of those with low virulence. Strains of particular 0-types were not more virulent per se, but among the serotypes, specific combinations of virulence factors appeared decisive, e.g., 018 HAVI B/D/G Hly+ K5+t- and 018 HAIIIIIVBN Hly- Cva +t- Kl +t- strains were, respectively, of high and low potential virulence. Isolates with high potential virulence were found to a similar extent in symptomatic and asymptomatic infections.},
  subject      = {Infektionsbiologie},
  language  = {en}
}