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

• Published in: Emerging infectious diseases Vol. 6; no. 5; pp. 458 - 465
• Main Authors: Kimmitt, P T, Harwood, C R, Barer, M R
• Format: Journal Article
• Language: English
• Published: United States U.S. National Center for Infectious Diseases 01.09.2000; Centers for Disease Control and Prevention
• Subjects: Anti-Bacterial Agents - pharmacology; antibiotics; Bacterial SOS Response; Bacteriophages; Bacteriophages - genetics; Diseases; Escherichia coli; Escherichia coli O157 - genetics; Escherichia coli O157 - metabolism; Gene Expression Regulation, Bacterial - drug effects; Genes, Reporter - drug effects; Humans; Lac Operon - drug effects; Lac Operon - genetics; phage production; Shiga toxin; Shiga Toxin - biosynthesis; Shiga Toxin - genetics; SOS-inducing antimicrobial agents; Toxins; United States; United States
• ISSN: 1080-6040; 1080-6059
• DOI: 10.3201/eid0605.000503

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.