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Where clinical symptoms were blank on the ESQ, we coded them as negative responses for these symptoms. We divided cases into 3 groups based on stx subtype: We used Fisher exact tests to compare proportions among different groups.
We assessed reporting of bloody diarrhea or hospitalization as a marker of disease severity by stx subtype. We performed all analyses in Stata Cases of Shiga toxin—producing Escherichia coli O H7 belonging to sublineage IIb, single-nucleotide polymorphism single linkage cluster This cluster comprised clinical isolates: H7 stx2a , 77 of stx- negative E.
H7 stx2c Figure 1 ; Technical Appendix Table. However, the number of cases of the stx- negative E. H7 clone has declined, whereas the stx2a and stx2c clones are increasing Figure 1.
Timed phylogeny of Shiga toxin—producing Escherichia coli O H7 sublineage IIb isolates illustrating the sequential loss of stx2c and subsequent gain of stx2a.
Scale bar indicates years in the past. We reconstructed a timed phylogeny of sublineage IIb Figure 2. This rate is less than the 2.
Historically, the majority of strains in sublineage IIb harbored a Stx2c-encoding prophage at sbcB , with the yehV SBI site occupied by a truncated non—Stx encoding prophage 5.
Analysis of the short read data indicated that in the stx- negative sublineage IIb clone, yehV was disrupted but sbcB was intact, indicating the loss of the Stx2c-encoding prophage from the SBI site.
The more recently emerged sublineage IIb stx2a clone had disrupted SBI sites at sbcB and yehV only, indicating that a Stx2a-encoding phage had been inserted into sbcB , the site left vacant in the stx- negative clone after the loss of stx2c.
H7 causing the infection Table 1. Rates of other symptoms varied; Hospitalization occurred more often for patients reporting bloody diarrhea No patients were known to experience HUS, and none died.
Among the clinical cases, Adult patients were infected with stx2a strains Conversely, children were more often infected with stx- negative strains than adults: There was also variation in stx subtype by sex; proportionately more female patients were infected with stx2a strains Adult patients reported bloody diarrhea The proportion of patients hospitalized did not differ significantly by sex or age group data not shown.
After adjusting for age adult or child and sex, the odds ratio of experiencing bloody diarrhea was significantly higher in those infected with the stx2a clone compared with patients infected with the stx -negative clone Table 2.
The odds of bloody diarrhea were no different for cases infected with the stx2c clone than for the stx -negative clone. Among the cases analyzed, being a child was protective for symptoms of bloody diarrhea.
The data described here support previous studies that showed the acquisition and loss of the Stx-encoding phage is highly dynamic in STEC O H7 stx2c progenitor, followed by the subsequent loss of stx2c in strains that acquired stx2a.
The involvement of a stx -negative intermediate in this process, as captured here, has not been previously described. The loss of the Stx2c-encoding phage appears to have facilitated the acquisition of the Stx2a-encoding phage because the latter was inserted into the same SBI site, sbcB , left vacant by the Stx2c-encoding phage.
Using phylogenetic analysis of variation at the whole-genome level, we reconstructed the recent evolutionary history of this emerging pathogenic clone within STEC O This clone has been associated with several outbreaks in the United Kingdom associated with a high incidence of HUS 10 , 21 — Here, we described an E.
H7 clone from yet another UK domestic lineage sublineage IIb that has recently acquired the Stx2a-encoding phage and is showing evidence of increasing pathogenic potential.
H7 within the same sublineage IIb cluster showed a significant association between the presence of stx2a and markers of disease severity; specifically, bloody diarrhea linked to higher rates of hospitalization.
Previous studies have reported evidence of increased pathogenicity of STEC harboring stx2a 4 , 5. However, these studies report on STEC from a wide range of different serotypes, exhibiting a wide variety of stx subtypes and are based on relatively small datasets.
In this study, we present the analysis of a large dataset focusing on a specific clade within a single serotype characterized by a limited number of stx subtype combinations, specifically stx2c , stx negative, and stx2a only.
This analysis enabled us to make direct comparisons between specific stx profiles while limiting the influence of other factors in the genome.
Strains of Stx-negative E. H7 are regarded as atypical enteropathogenic E. In this study, the fact that clinical cases infected with the E.
H7 stx -negative clone reported a similar frequency of symptoms, including bloody diarrhea and hospitalization, as those infected with STEC O H7 stx2c despite the loss of stx was an unexpected finding that requires further investigation.
A timed phylogenetic reconstruction of the evolutionary history of a cluster of sublineage IIb charted the recent emergence of a highly pathogenic clone of STEC O The symptom of bloody diarrhea, a marker of severity and predictor of HUS development 2 , was strongly associated with cases infected with isolates of STEC O H7 harboring stx2a compared with those isolates without stx or those with stx2c.
Our analysis also illustrated the highly dynamic nature of the Stx-encoding phages. In contrast to the observed excision events of stx2c -encoding phages in O H7, there is evidence to suggest that once a Stx2a-encoding phage is integrated into a population it tends to be maintained 5.
H7 acquiring stx2a is of public health concern. H7 WGS surveillance data have a role in monitoring and anticipating emerging threats to public health and in contributing to our understanding of the underlying pathogenic mechanisms associated with severe gastrointestinal illness.
Her interests include public health surveillance of STEC and hemolytic uremic syndrome and the investigation of outbreaks of foodborne gastrointestinal disease.
Table of Contents — Volume 24, Number 12—December Please use the form below to submit correspondence to the authors or contact them at the following address:.
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