Anti-Shiga Toxin 2 polyclonal antibody

How pathogens evolve their virulence to humans in nature is a scientific issue of great medical and biological importance. Shiga toxin (Stx)-producing Escherichia coli (STEC) and enteropathogenic E. coli (EPEC) are the major foodborne pathogens that can cause hemolytic uremic syndrome and infantile diarrhea, respectively. The locus of enterocyte effacement (LEE)-ncoded type 3 secretion system (T3SS) is the major virulence determinant of EPEC and is also possessed by major STEC lineages. Cattle are thought to be the primary reservoir of STEC and EPEC. However, genome sequences of bovine commensal E. coli are limited, and the emerging process of STEC and EPEC is largely unknown. Here, we performed a large-scale genomic comparison of bovine commensal E. coli with human commensal and clinical strains, including EPEC and STEC, at a global level. The analyses identified two distinct lineages, in which bovine and human commensal strains are enriched, respectively, and revealed that STEC and EPEC strains have emerged in multiple sublineages of the bovine-associated lineage. In addition to the bovine-associated lineage-specific genes, including fimbriae, capsule, and nutrition utilization genes, specific virulence gene communities have been accumulated in stx-and LEE-positive strains, respectively, with notable overlaps of community members. Functional associations of these genes probably confer benefits to these E. coli strains in inhabiting and/or adapting to the bovine intestinal environment and drive their evolution to highly virulent human pathogens under the bovine-adapted genetic background. Our data highlight the importance of large-scale genome sequencing of animal strains in the studies of zoonotic pathogens.

Cattle are a reservoir for enterohemorrhagic Escherichia coli (EHEC), and ground beef is a major vehicle for human infection with EHEC. Heat resistance of E. coli, including EHEC, is impacted by NaCl and other additives. This study aimed to evaluate the effect of NaCl and other additives on the heat resistance of E. coli in beef patties. E. coli AW1.7 Delta pHR1(pLHR) with the locus of heat resistance (LHR), E. coli AW1.7 Delta pHR1(pRK767) without LHR, or a 5-strain cocktail of EHEC were inoculated (10(7)-10(8) CFU/g) into ground beef (15% fat) with NaCl (0-3%), marinade, carvacrol (0.1%), potassium lactate (3%) or chitosan (0.1%) following different protocols. Patties were grilled immediately, or stored in sterile bags for two days at 4 degrees C prior to grilling to a core temperature of 71 degrees C. Cell counts of LHR-positive E. coli AW1.7 Delta pHR1(pLHR) were higher than that of the isogenic LHR-negative E. coli AW1.7 Delta pHR1(pRK767) by > 3 log(10) (CFU/g) after cooking. Addition of 3% NaCl increased survival of E. coli AW1.7 Delta pHR1(pRK767) and the EHEC cocktail while cell counts of the heat resistant strains were not changed. A protective effect of NaCl was not observed with E. coli AW1.7 Delta pHR1(pRK767) or EHEC if cells of E. coli were cooled to 4 degrees C prior to mixing with cold meat and NaCl, indicating that the response of E. coli to osmotic shock contributes to this effect. Chitosan enhanced the thermal destruction of LHR-positive E. coli AW1.7 Delta pHR1(pLHR) in ground beef stored at 4 degrees C for 2 days, while marinade, carvacrol, or potassium lactate had no such effect, indicating that chitosan can be characterized as an effective hurdle concept to reduce the potential risk of LHR-positive pathogen to meat safety.