In 2009, an outbreak of enterohemorrhagic Escherichia coli (EHEC) on an open farm infected 93 persons, and approximately 22% of these individuals developed hemolytic-uremic syndrome (HUS). Genome sequencing was used to investigate outbreakderived animal and human EHEC isolates. Phylogeny based on the whole-genome sequence was used to place outbreak isolates in the context of the overall E. coli species and the O157:H7 sequence type 11 (ST11) subgroup. Four informative single nucleotide polymorphisms (SNPs) were identified and used to design an assay to type 122 other outbreak isolates. The SNP phylogeny demonstrated that the outbreak strain was from a lineage distinct from previously reported O157:H7 ST11 EHEC and was not a member of the hypervirulent clade 8. The strain harbored determinants for two Stx2 verotoxins and other putative virulence factors. When linked to the epidemiological information, the sequence data indicate that gross contamination of a single outbreak strain occurred across the farm prior to the first clinical report of HUS. The most likely explanation for these results is that a single successful strain of EHEC spread from a single introduction through the farm by clonal expansion and that contamination of the environment (including the possible colonization of several animals) led ultimately to human cases.

SUMMARYIn the summer of 2009, an outbreak of verocytotoxigenic Escherichia coli O157 (VTEC O157) was identified in visitors to a large petting farm in South East England. The peak attack rate was 6/1000 visitors, and highest in those aged <2 years (16/1000). We conducted a case-control study with associated microbiological investigations, on human, animal and environmental samples. We identified 93 cases; 65 primary, 13 secondary and 15 asymptomatic. Cases were more likely to have visited a specific barn, stayed for prolonged periods and be infrequent farm visitors. The causative organism was identified as VTEC O157 PT21/28 with the same VNTR profile as that isolated in faecal specimens from farm animals and the physical environment, mostly in the same barn. Contact with farm livestock, especially ruminants, should be urgently reviewed at the earliest suspicion of a farm-related VTEC O157 outbreak and appropriate risk management procedures implemented without delay.

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ObjectivesHaemolytic uraemic syndrome (HUS) following Shiga toxin-producing Escherichia coli (STEC) infection is the the most common cause of acute renal failure among children in the UK. This study explored differential progression from STEC to HUS by social, demographic and clinical risk factors.MethodsWe undertook a retrospective cohort study linking two datasets. We extracted data on paediatric STEC and HUS cases identified in the Public Health England National Enhanced Surveillance System for STEC and British Paediatric Surveillance Unit HUS surveillance from 1 October 2011 to 31 October 2014. Using logistic regression, we estimated the odds of HUS progression by risk factors.Results1059 paediatric STEC cases were included in the study, of which 207 (19.55%, 95% CI 17% to 22%) developed HUS. In the fully adjusted model, the odds of progression to HUS were highest in those aged 1–4 years (OR 4.93, 95% CI 2.30 to 10.56, compared with 10–15 years), were infected with an Shiga toxin (stx) 2-only strain (OR 5.92, 95% CI 2.49 to 14.10), were prescribed antibiotics (OR 8.46, 95% CI 4.71 to 15.18) and had bloody diarrhoea (OR 3.56, 95% CI 2.04 to 6.24) or vomiting (OR 4.47, 95% CI 2.62 to 7.63), but there was no association with progression to HUS by socioeconomic circumstances or rurality.ConclusionCombining data from an active clinical surveillance system for HUS with the national enhanced STEC surveillance system suggests that 20% of diagnosed paediatric STEC infections in England resulted in HUS. No relationship was found with socioeconomic status or rurality of cases, but differences were demonstrated by age, stx type and presenting symptoms.