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Toxin gene expression by shiga toxin-producing Escherichia coli: the role of antibiotics and the bacterial SOS response.

Supporting Files Public Domain
File Language:
English


Details

  • Alternative Title:
    Emerg Infect Dis
  • Personal Author:
  • Description:
    Toxin synthesis by Shiga toxin-producing Escherichia coli (STEC) appears to be coregulated through induction of the integrated bacteriophage that encodes the toxin gene. Phage production is linked to induction of the bacterial SOS response, a ubiquitous response to DNA damage. SOS-inducing antimicrobial agents, particularly the quinolones, trimethoprim, and furazolidone, were shown to induce toxin gene expression in studies of their effects on a reporter STEC strain carrying a chromosome-based stx2::lacZ transcriptional fusion. At antimicrobial levels above those required to inhibit bacterial replication, these agents are potent inducers (up to 140-fold) of the transcription of type 2 Shiga toxin genes (stx2); therefore, they should be avoided in treating patients with potential or confirmed STEC infections. Other agents (20 studied) and incubation conditions produced significant but less striking effects on stx2 transcription; positive and negative influences were observed. SOS-mediated induction of toxin synthesis also provides a mechanism that could exacerbate STEC infections and increase dissemination of stx genes. These features and the use of SOS-inducing antibiotics in clinical practice and animal husbandry may account for the recent emergence of STEC disease.
  • Subjects:
  • Source:
    Emerg Infect Dis. 6(5):458-465.
  • Document Type:
  • Volume:
    6
  • Issue:
    5
  • Collection(s):
  • Main Document Checksum:
    urn:sha256:f2a5def0327acb8c30624ba65798b69b50cc39ecc4302dd9155943f8f3d8fe8c
  • Download URL:
  • File Type:
    Filetype[PDF - 145.16 KB ]
File Language:
English
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