Dynamics of insertion sequence element IS629 inactivation of verotoxin 2 genes in Escherichia coli O157:H7. Issue 8 (11th April 2017)

• Record Type: Journal Article
• Authors: Loftsdóttir, Heiður; Söderlund, Robert; Jinnerot, Tomas; Eriksson, Erik; Bongcam-Rudloff, Erik; Aspán, Anna
• Is Part Of: FEMS microbiology letters. Volume 364:Issue 8(2017)
• Publication Date: 2017-04-11
• Subjects: O157:H7 -- IS629 -- VTEC -- STEC -- verotoxin -- digital PCR; Microbiology -- Periodicals; 579
• DOI: 10.1093/femsle/fnx074
• Languages: English
• ISSNs: 0378-1097

Abstract

Abstract: There are several anecdotal reports of insertion sequence (IS) element inactivation of verotoxin genes among enterohaemorrhagic Escherichia coli of the serotype O157:H7, a pathogen causing severe gastrointestinal disease in infected humans. These insertions can be expected to drastically reduce the virulence of the bacteria. IS element inactivation has been shown to be reversible in model systems, suggesting the possibility of spontaneous restoration of virulence. In this study, traditional and high-throughput sequencing was used to characterise three patterns of IS 629 inactivation of verotoxin 2 genes in EHEC O157:H7, caused by insertion or insertion followed by partial deletion. At least one of the patterns of inactivation appears to have persisted several years among cattle O157:H7, indicating it has no major effect on fitness in the animal reservoir. Digital PCR was used to directly quantify the reversal rates of the insertional inactivation of a selected isolate under laboratory conditions. Inserts were found to be absent from in the order of 1/10 5 of individual genomes, with significantly higher loss frequencies observed in cultures under nutrient-poor conditions. We conclude that strains with this type of inactivation found in food or animal samples should be considered a threat to human health, and may pose a challenge for PCR-based detection methods. Abstract : A latent ability of certain Escherichia coli bacteria to cause severe disease in humans can be re-activated due to the movements of small mobile DNA elements.