Cloned hemolysin genes from Escherichia coli that cause urinary tract infection determine different levels of toxicity in mice.
After intraperitoneal injection of mice with Escherichia coli strains isolated from patients with urinary tract infections, the mortality due to hemolytic (Hly+) and nonhemolytic (Hly-) isolates was 77 and 40%, respectively. Deletion of the chromosomal hemolysin (hly) determinant in an E. coli O6: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 pHly152-encoded hly determinant into the Hly- E. coli O6 mutant strain increased toxicity by only a marginal degree, transformation with the cloned chromosomal hly determinants from two E. coli strains of serotypes O18ac:K5:H- and O75:K95:H? resulted in markedly greater toxicity, even exceeding that of the original Hly+ E. coli O6 wild-type strain.
D000818:Animals; D003001:Cloning, Molecular; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000382:microbiology; D005798:Genes, Bacterial; D006459:Hemolysin Factors; D006460:Hemolysin Proteins / Q000235:genetics*; D051379:Mice; D009154:Mutation; D010957:Plasmids; D014169:Transformation, Bacterial; D014552:Urinary Tract Infections / Q000382:microbiology; D014774:Virulence
D006460:Hemolysin Proteins