RESUMEN
Shiga toxin-producing Escherichia coli (STEC) can cause severe clinical disease in humans, particularly in young children. Recent advances have led to greater availability of sequencing technologies. We sought to use whole genome sequencing data to identify the presence or absence of known virulence factors in all clinical isolates submitted to our laboratory from Southern Alberta dated 2020-2022 and correlate these virulence factors with clinical outcomes obtained through chart review. Overall, the majority of HUS and hospitalizations were seen in patients with O157:H7 serotypes, and HUS cases were primarily in young children. The frequency of virulence factors differed between O157:H7 and non-O157 serotypes. Within the O157:H7 cases, certain virulence factors, including espP, espX1, and katP, were more frequent in HUS cases. The number of samples was too low to determine statistical significance.
RESUMEN
Non-O157 serogroups contribute significantly to the burden of disease caused by Shiga toxin-producing Escherichia coli (STEC) and have been underrecognized by traditional detection algorithms. We described the epidemiology of non-O157 STEC in Alberta, Canada for the period of 2018 to 2021. All non-O157 STEC isolated from clinical samples were submitted for serotyping and qPCR targeting the stx1 and stx2 genes. A total of 729 isolates were identified. Increased detection occurred over the summer months, peaking in July. Patients 18 years and younger made up 42.4% of cases, with 31.1% in those 0-9 years of age. There was a slight female predominance (399/729, 54.7%) A total of 50 different serogroups were detected; the most common were O26 (30.3%), O103 (15.9%), O111 (12.8%), O121 (11.0%), O118 (3.3%) and O71 (2.9%). These six serogroups made up 76.2% of all isolates. In total, 567 (77.8%) were positive for stx1, 114 (15.6%) were positive for stx2 and 48 (6.6%) were positive for both stx1 and stx2. A wide variety of non-O157 serogroups have been detected in Alberta, with the most frequent serogroups differing from other locations. These results highlight the need for further characterization of their virulence factors and clinical impact.
RESUMEN
The purpose of this study was to identify Escherichia coli isolates obtained from patients experiencing acute gastroenteritis that possess the locus of heat resistance (LHR) and characterize their heat resistance upon exposure to temperatures of 60 °C and 71 °C. From a collection of 613 clinical E. coli strains, 3 heat resistant E. coli isolates were identified. Two of the 3 isolates were stx1 positive; no isolates possessed stx2 as determined by qPCR. D60-values of heat resistant isolates all exceeded 10.20 min with one isolate's D60-values ranging from 20.46 to 72.47 min. The presence of 4% additional NaCl significantly increased D60-values of 2 clinical isolates. Cell reductions of heat resistant isolates in ground beef patties grilled to 60 °C and 71 °C remained above 2.8 and 4.9 log CFU/mL, respectively, compared to reductions of 6.1 log CFU/mL and greater in heat sensitive E. coli. Constitutive expression of novel Clp protease ClpK, encoded on open reading frame 3 of the LHR, was identified in all heat resistant isolates by SDS-PAGE and peptide mass fingerprinting. This data is the first to report heat resistant E. coli possessing the LHR involved in clinical infection, highlighting the potential threat of heat resistant enteric pathogens on food safety.