Abstract
In this study, 140 cattle STEC isolates belonging to serogroups O157, O26, O145, O121, O103 and O45 were characterized for 38 virulence-associated genes, antimicrobial resistance profiles and genotyped by PFGE. The majority of isolates carried both stx1 and stx2 concurrently, stx2c, and stx2d; plasmid-encoded genes ehxA, espP, subA and saa but lacked katP and etpD and eaeA. Possession of eaeA was significantly associated with the presence of nle genes, katP, etpD, ureC and terC. However, saa and subA, stx1c and stx1d were only detected in eaeA negative isolates. A complete OI-122 and most non-LEE effector genes were detected in only two eaeA positive serotypes, including STEC O157:H7 and O103:H2. The eaeA gene was detected in STEC serotypes that are commonly implicated in severe humans disease and outbreaks including STEC O157:H7, STEC O145:H28 and O103:H2. PFGE revealed that the isolates were highly diverse with very low rates of antimicrobial resistance. In conclusion, only a small number of cattle STEC serotypes that possessed eaeA, had the highest number of virulence-associated genes, indicative of their high virulence. Further characterization of STEC O157:H7, STEC O145:H28 and O103:H2 using whole genome sequencing will be needed to fully understand their virulence potential for humans.
Highlights
Shiga toxin-producing Escherichia coli (STEC) are zoonotic food-borne pathogens characterized by mild to severe diarrhea, hemorrhagic colitis (HC) and the hemolytic uremic syndrome (HUS), a leading cause of acute renal failure in young children and the elderly[1]
Intimin is encoded on the locus of enterocyte effacement (LEE), and is responsible for intimate attachment of eaeA-positive STEC strains to the host intestinal mucosa and formation of typical attaching and effacing (A/E) lesions commonly observed in STEC disease[8]
Since the first report on foodborne STEC in humans nearly 40 years ago, a number of studies have been published on virulence, antimicrobial resistance and molecular epidemiology of STEC around the world
Summary
Shiga toxin-producing Escherichia coli (STEC) are zoonotic food-borne pathogens characterized by mild to severe diarrhea, hemorrhagic colitis (HC) and the hemolytic uremic syndrome (HUS), a leading cause of acute renal failure in young children and the elderly[1]. STEC serogroups O26, O45, O103, O111, O121, O145, and O157 are frequently associated with severe illness and outbreaks in humans[3], and colloquially termed the “top or big 7” Another important virulence factor of STEC is intimin (eaeA)[8]. Several STEC O-islands (OIs), including OI-122, OI-57, OI-71 OI-36 and OI-43/48 encode genes, which are absent in nonpathogenic E. coli and are considered STEC virulence-associated genes[17] These genes have been used in molecular risk assessment studies to classify STEC serotypes into different seropathotypes based on whether a particular serotype has been implicated in mild, severe illness or no disease at all in humans[18,19]. Non-LEE effectors have been associated with different functions including immunosuppression, adherence, invasion, colonization of host enterocytes, disruption of tight junctions and protein trafficking in the host[18,19,30,33]
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