|PATEL, ISHA - Us Food & Drug Administration (FDA)|
|JACKSON, SCOTT - Us Food & Drug Administration (FDA)|
|LECLERC, J - Us Food & Drug Administration (FDA)|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2011
Publication Date: N/A
Technical Abstract: Shiga toxin-producing Escherichia coli (STEC) O157:H7 and non-O157 serogroups are a common cause of outbreaks of human illness; however, few studies have systematically collected and verified reliable biomarkers to enable detection and differentiation of highly pathogenic STEC. The goal of this study was to use comparative genomics approaches to identify biomarkers and determine the presence of virulence factors, including genes on pathogenicity islands (PAIs) and other mobile genetic elements.This work involved data mining of information from the NCBI Entrez Genome Project database and the European Nucleotide Archive (ENA), and text mining of published literature. A custom Affymetrix-FDA ECSG microarray, representing 32 E. coli and Shigella genome sequences, as well as 46 plasmid sequences, was also used for comparative genomic hybridization analysis of O157, O26, O111, O145, O103, O121, O45, O91, and O113 STEC strains. Data verification and validation were implemented by the Standalone BLAST program. PAI irp2-fyuA, the HPI element mainly associated with serotype O26, did not exist in tested O157:H7 isolates. Several PAIs, including PAI-43, 47, 154, prophage CPI-933-H-I, and the highly variable regions of the O-antigen cluster PAI-84 were identified to be O157:H7 specific. Also, a previously characterized type II protein secretion pathway found in the prototypic human ETEC O78:H11 strain H10407 was not identified in sequenced STEC strains. In this report, we show that genes encoding for some important plasmid-encoded virulence factors, including toxins, hemolysin, Etp, and EspP are not always found in strains of the same serotype. Studies are underway to further correlate the presence of specific PAIs and virulence genes to highly pathogenic STEC strains.