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

Lookup NU author(s): Dr Patrick Kimmitt, Professor Colin Harwood, Dr Michael Barer


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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.

Publication metadata

Author(s): Kimmitt PT, Harwood CR, Barer MR

Publication type: Article

Publication status: Published

Journal: Emerging Infectious Diseases

Year: 2000

Volume: 6

Issue: 5

Pages: 458-465

ISSN (print): 1080-6040

ISSN (electronic): 1080-6059

Publisher: U.S. Department of Health and Human Services


DOI: 10.3201/eid0605.000503

PubMed id: 10998375


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