Browse by author
Lookup NU author(s): Dr Patrick Kimmitt, Professor Colin Harwood, Dr Michael Barer
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
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.
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
URL: http://dx.doi.org/10.3201/eid0605.000503
DOI: 10.3201/eid0605.000503
PubMed id: 10998375
Altmetrics provided by Altmetric
