Submitted to: American Society of Microbiologists Abstracts
Publication Type: Abstract only
Publication Acceptance Date: 12/12/2001
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Shiga-toxin producing E. coli (STEC) are capable of causing hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS) in humans. E. coli O157:H7 is the STEC responsible for the majority of HC and HUS outcomes in the U.S. with serotypes O26, O103, O111 and others responsible for rare disease occurrences. While E coli O157:H7 causes most human STEC disease, evidence suggests that the isolation rates of non-O157 STEC from animal feces are higher than those of E. coli O157:H7. In order to understand the genetic differences between STEC O157:H7 and non-O157 STEC, we performed sample sequencing on three STEC, O157:H7, O111:NM, and O26:NM, isolated from bovine feces. A random total genomic library was generated from each serotype and sequenced to produce at least a 1X coverage of a 6 megabase genome. Local homology searches were performed using blastn against the complete genomes of E. coli K-12 (U00096), E. coli O157:H7 EDL 933 (AE005174) and E. coli O157:H7 Sakai (BA000007). Sequences were also subjected to local blastx homology searches using the nr database. The E. coli O157:H7 isolate contains three sequencing reads that are different from the published E. coli O157:H7 genome sequences. The O111:nm isolate had 216 sequencing reads and O26:nm isolate had 366 sequencing reads that had no match by blastn or blastx. By comparing the genomic content of different shiga-toxin producing E. coli, we hope to better define the unique and essential elements of STEC.