Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/22211
Title: Toxin gene expression by shiga toxin-producing Escherichia coli: the role of antibiotics and the bacterial SOS response
Authors: Kimmitt, P. T.
Harwood, C. R.
Barer, M. R.
First Published: Sep-2000
Citation: Emerging Infectious Diseases, 2000, 6 (5), pp. 458-465
Abstract: 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.
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.
DOI Link: 10.3201/eid0605.000503
ISSN: 1080-6040
eISSN: 1080-6059
Links: http://hdl.handle.net/2381/22211
http://wwwnc.cdc.gov/eid/article/6/5/00-0503_article
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Emerging Infectious Diseases is published by the Centers for Disease Control and Prevention, a U.S. Government agency. Therefore, all materials published in Emerging Infectious Diseases are in the public domain and can be used without permission. Proper citation, however, is required.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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