![]() coli (STEC) however, STEC encompass both LEE-positive (typical EHEC) and LEE-negative (atypical EHEC) E. EHEC also fall under the category of Shiga toxin-producing E. However, EHEC differ from EPEC in that they possess phage-associated Shiga toxins ( stx), which contribute to the hemorrhagic colitis and hemolytic uremic syndrome (HUS) associated with EHEC infections ( Mayer et al., 2012). nle genes are frequently carried on prophage elements and contribute to virulence by interfering with host signaling pathways, apoptosis and phagocytosis ( Wong et al., 2011) as well as disrupting host cell cytoskeleton and tight junctions ( Gomes et al., 2016). In addition to the LEE, EHEC and EPEC possess various non-LEE ( nle)-encoded effector genes. coli confers A/E lesion activity ( McDaniel and Kaper, 1997). The genes located within the LEE are sufficient for A/E lesion formation, as transferring LEE to commensal E. The LEE enables EPEC and EHEC to adhere intimately to intestinal epithelial cells and cause attaching and effacing (A/E) lesions leading to diarrheal illness ( Kaper et al., 2004). coli (EPEC) are DEC pathotypes that share a common mechanism of pathogenesis defined in part by the carriage of a chromosomally located pathogenicity island (PAI) termed the locus of enterocyte effacement (LEE). coli (DEC) and are classified into pathotypes according to specific virulence factors and ensuing clinical manifestations ( Gomes et al., 2016).Įnterohemorrhagic E. coli that induce intestinal disease are known as diarrheagenic E. ![]() coli genomes allows for some strains to exist as gastrointestinal tract commensals, while the acquisition of different combinations of virulence-associated genes (VAGs) has generated clades that cause a diverse range of intestinal and extraintestinal illnesses ( Tenaillon et al., 2010). coli ST302 strains and informs AMR genomic surveillance.Įscherichia coli is a versatile Gram-negative bacterium whose genome is shaped by lateral gene transfer. This study sheds light on the virulence and AMR potential of E. F2_18C was shown to carry two additional pathogenicity islands – ETT2, and the STEC-associated PAI CL 3, plasmid-associated heavy metal resistance genes, as well as several unoccupied stx-phage attachment sites. A comparison of 33 HI2:ST3 plasmids demonstrated that those of Australian origin have not acquired resistances to extended-spectrum beta-lactams, colistin, fosfomycin or rifampicin, unlike those originating from Asia. Plasmid comparisons showed that pF2_18C_FIB shared homology with EHEC virulence plasmids such as pO103 while pF2_18C_HI2 is a large multidrug resistance IncHI2:ST3 plasmid. ![]() coli ST302 strains carry diverse VAGs, including those that typically associated with extraintestinal pathogenic E. coli ST302 strains and short-read gene screens were used to compare their virulence-associated gene (VAG) and antimicrobial resistance gene (ARG) cargo. ![]() Public databases were interrogated for WGSs of E. coli ST302 strains in proximity to EHEC ST32 (O145:H28) strains. Through WGS and hybrid assembly we present the first closed chromosome, and two circularized plasmids of an ST302 strain - F2_18C, isolated from a healthy pig in Australia. Escherichia coli ST302 (O108:H9, O182:H9, O45:H9) are aEPEC that have been isolated from diarrheic human, pig and rabbit hosts, as well as in healthy pigs, however, no study to date has focused on E. While aEPEC can cause disease outright, the potential to acquire stx, one of the most potent bacterial toxins known, merits close monitoring. However, phylogenetic analyses often associate aEPEC with EHEC, promoting the hypothesis that aEPEC are the progenitors of EHEC, which is supported by aEPEC conversion to EHEC by stx-carrying phages. They are differentiated from typical EPEC by the lack of bundle-forming pili, and from EHEC by the lack of phage-mediated stx toxins. 3NSW Department of Primary Industries, Elizabeth MacArthur Agricultural Institute, Menangle, NSW, AustraliaĪEPEC are associated with persistent diarrhea, and diarrheal outbreaks in both humans and animals worldwide.2Australian Centre for Genomic Epidemiological Microbiology, University of Technology Sydney, Sydney, NSW, Australia.1ithree institute, University of Technology Sydney, Sydney, NSW, Australia.
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