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E. COLI EHEC - UK (03): (ENGLAND) O55, 2014-2015

E. COLI EHEC - UK (03): (ENGLAND) O55, 2014-2015

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A ProMED-mail post <http://www.promedmail.org> ProMED-mail is a program of the International Society for Infectious Diseases <http://www.isid.org>

Date: Thu 7 Sep 2017
Source: Eurosurveillance, Volume 22, Issue 36 [edited] <http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=22872>


Recurrent seasonal outbreak of an emerging serotype of Shiga toxin-producing _E. coli_ (STEC O55:H7 Stx2a) in the south west of England
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Shiga toxin-producing _Escherichia coli_ (STEC [also known as enterohemorrhagic _E. coli_, EHEC. - Mod.LL]) is known to cause self-limiting diarrhoeal illness, sometimes bloody diarrhoea and complications such as hemorrhagic colitis and hemolytic uraemic syndrome (HUS) (1-3). EHEC O157:H7 is the most common serotype in England while the incidence of non-O157 EHEC serotypes such as O26, O45, O103, O111, O121 and O145, some of which have been implicated in a number of outbreaks internationally (4-8), may be under-reported in the English national surveillance system run by Public Health England (PHE). This is due to the lack of general applicability of current culture-based detection methods (9,10).

The signal
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PHE South East Centre was notified in July 2014 of 2 children with HUS in the county of Dorset. Further cases, all living in Dorset, were identified during the following months, including an outbreak at a nursery. Fecal specimens tested at the local hospital laboratory were negative for EHEC O157. Further testing at the Gastrointestinal Bacterial Reference Unit (GBRU) PHE, Colindale, London, identified the causative organism as EHEC O55:H7 which carried the Shiga toxin gene (stx2) and the intimin-encoding gene eae (_E. coli_ attaching and effacing). The combination of these virulence genes is associated with an elevated risk of HUS (11). Phylogenetic analysis using whole genome sequencing (WGS) has indicated EHEC O55:H7 to be the ancestor of the highly pathogenic clone EHEC O157:H7 (12).

The reference laboratory in the Republic of Ireland (ROI) routinely sends a sub-set of non-O157 EHEC to GBRU for serotyping. A search of GBRU's database, following detection of the EHEC non-O157-related HUS cases in Dorset, revealed that 9 cases of EHEC O55:H7 had occurred in ROI between 2012 and 2014. However, prior to July 2014 EHEC O55:H7 had not been isolated from human cases or animals in England. The outbreak starting in July 2014 was, therefore, the 1st known outbreak in England of EHEC O55:H7 causing severe illness.

Apart from human-to-human transmission, we considered 3 competing hypotheses based on established (13) EHEC O55:H7 transmission pathways: (i) consumption of contaminated food or drinking water; (ii) specific recreational or environmental exposure; (iii) epizootic vector and/or general environmental contamination. The objectives of our investigation were case finding, investigating the source and controlling the outbreak.

Methods [except for the microbiological methods, see original URL. - Mod.LL]
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Microbiological investigations:

Case finding - Prior to the identification of EHEC O55:H7 as the etiological agent of this outbreak, serum samples from initial cases with HUS that were culture negative for EHEC O157 were assessed for the presence of antibodies to the LPS of non-O157 serogroups (O26, O55, O103, O111, O128 and O145) at GBRU in PHE Colindale (16). Fecal specimens were tested using PCR (17) at GBRU for the presence of 6 genes and cultured on MacConkey, Sorbitol MacConkey (SMAC) and cefixime-tellurite SMAC (CTSMAC) agar. For all positive specimens, 10 colonies were retested using the same PCR. Those colonies testing positive for stx were identified biochemically, serotyped and characterised by additional PCR assays (17). EHEC guidelines (18) recommend testing fecal specimens for non-O157 EHEC from HUS patients, cases of bloody diarrhea where STEC is suspected, and stx PCR-positive fecal specimens at the local hospital laboratory. All close contacts of cases were screened via testing of serum and/or faecal specimens, including all children and staff in a nursery cluster.

From December 2014 to January 2015 and again from June 2015, active case finding included screening of fecal specimens from all individuals with bloody diarrhoea by Dorset laboratories, with prospective referral of negative specimens to GBRU for additional testing. In August 2015, enhanced testing was introduced in one Dorset laboratory and by October 2015, this was replicated in the remaining 2 laboratories and the PHE Specialist Laboratory in Southampton. This involved a 12-week extended testing regime, which analysed specimens from both primary and secondary care, with all diarrhoeal specimens tested using an additional MacConkey Agar with Sorbitol (SMAC) agar plate. Any non-sorbitol fermenting isolates of E. coli were sent to GBRU for further characterisation and typing.

Food, water and environmental specimens - Animal fecal specimens were analysed by GBRU using the same protocol as for human fecal specimens. All other samples were analysed by PHE's Food, Water and Environmental (FWE) Microbiology laboratories. At FWE, real-time PCR was used to examine samples for the presence of EHEC based on CEN/ISO TS 13136 (19). Water samples (up to 1 L) were filtered and filtrates enriched in 100 mL Modified Tryptone Soya Broth (mTSB). Bootsocks were immersed in 250 mL mTSB and swabs were immersed in 90 mL mTSB. Enrichment broths that were PCR-positive for stx were sub-cultured onto MacConkey and SMAC agar and up to 50 colonies retested using the same PCR assay. Any STEC strains isolated were sent to GBRU for further characterisation.

Whole genome sequencing - All isolates of EHEC O55:H7 from this outbreak cultured from 24 human and two animal fecal specimens together with 11 background EHEC O55:H7 isolates from ROI contained within the PHE archive were whole genome sequenced by PHE Genome Sequencing Unit using Nextera library preparation on the Illumina HiSeq 2500 run in fast mode according to the manufacturers' instructions [20]. All sequences were mapped against the sequence of the _E. coli_ O55:H7 reference strain CB9615 (GenBank accession number: CP001846.1) using BWA-MEM (19). SNPs were identified using GATK2 (21) in unified genotyper mode. Core genome positions that had a high quality SNP (over 90 percent consensus, minimum depth 10x, MQ ≥ 30) in at least one strain were extracted and RaxML (21) used to derive the maximum likelihood phylogeny of the isolates under the GTRCAT model of evolution. FASTQ reads from all sequences in this study can be found at the PHE Pathogens BioProject at the National Center for Biotechnology Information (accession number: PRJNA315192).

International investigations:

The public health team in the ROI administered the PHE EHEC questionnaire to earlier Irish cases and provided additional information on demographics and shared exposures of these cases. Postcodes of the primary cases in Dorset and the counties where infected individuals reside in ROI were taken as points of reference to examine both large scale migration and smaller regional movements of different migratory bird species using the British Trust for Ornithology mapping tool (22). Live cattle movements between ROI and Dorset in 2013 and 2014 were mapped by date of movement and the postcode of the recipient farms/markets.

Results
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Epidemiological investigation:

From July 2014 to September 2015 we identified 31 confirmed cases; 28 were associated with six epidemiological clusters (Table [for Tables and figures, see original URL. - Mod.LL]), with one cluster (family B) arising due to 2 (co)primary cases with symptom onset on the same day. Symptom onset was seasonal, occurring between July and November 2014 and May to September 2015 (Figure 1). There were 3 probable cases associated with the nursery and no probable community cases.

Of 21 cases symptomatic with HUS, bloody diarrhea or diarrhea (21/31), 18 were confirmed on fecal culture and three by serology. Of the 10 asymptomatic cases (10/31), 6 were culture-positive and 4 were identified by serology. A total of 20 of the 31 cases were children, 16 were below the age of 5 years and 11 of the 20 children developed HUS (Table). Across all cases, HUS was more common (13/31) than expected for EHEC O157 (172/3,323; 5 percent, chi-squared p less than 0.0001) (2).

The network analysis revealed 9 of the 10 (co)primary cases had domestic contact with cats (5/10) and/or dogs (5/10). In addition to domestic animal contact, the only common factor among the (co)primary cases was residing in or around, or having links to, Bournemouth and Weymouth in Dorset.

Nursery cluster - 12 cases (of whom 6 were symptomatic) were associated with a nursery (Figure 1, Table), including staff, children and their household contacts. As many as 12 staff members in the nursery responded to the staff questionnaire (12/30), revealing a history of diarrhea in 3 screen-negative staff in the previous month including one with a family connection to a confirmed case. Questionnaires on nursery children had a poor response rate of 14 percent but identified a child that may have been previously symptomatic. A total of 6 cases in children (2 symptomatic) were identified from the 99 of 112 staff members and children screened. An additional 3 children were identified who were culture-negative but PCR positive for the eae (intimin) gene only, meaning they were defined as probable cases at the point of screening. One of these 3 children had been previously symptomatic and had a delay of ten days between symptom onset and specimen collection.

The delay between symptom onset and specimen collection for the confirmed nursery cases ranged from 0 to 9 days (mean: 5 days). The optimum time for testing is as soon as possible after onset however 5 days is still a satisfactory timeframe as PCR is able to detect dead bacteria. The investigation did not reveal any possible food or environmental sources of transmission at the nursery and no epidemiological links were identified between the primary nursery and primary community cases.

Environmental investigation:

Food, water, environmental and animal samples - No EHEC O55:H7 was isolated from over 100 food, water and environmental samples or from 17 animal samples from the petting farm. EHEC O55:H7 was isolated from a cat fecal specimen, taken from a concrete path outside the home of the primary case in Family C (Case 22). The pet cat of this household had been ill but tested negative. All pets of (co)primary cases tested retrospectively following this finding yielded negative results but the faeces of a symptomatic pet cat, tested prospectively, was positive for EHEC O55:H7. This cat belonged to case 26, who was not associated with an epidemiological cluster, and the cat's illness preceded symptom onset in the case. These 2 positive cat specimens were taken about 4.5 km [approx. 2.8 mi] and 2 months apart.

Food chain analysis - The food chain analysis did not identify any product lines that were sourced specifically for retailers in the Dorset area. No links were identified between the premises investigated, including 2 nurseries, 2 petting farms, a local butcher, an abattoir, a café, takeaway restaurants, mobile food vans and a national chain of restaurants. There were no significant commonalities between food items consumed by the pets and all pet food brands reported had national distribution networks.

Hydrological data analysis - 4 media reports of flooding events and 2 additional theoretical flooding events were identified during the period from December 2014 to September 2015. After excluding one theoretical event which occurred during January 2015 when there were no cases, the remaining 5 flooding events occurred 1-9 days (median: 8 days) before symptom onset among 5 of the 6 (co)primary cases linked to Bournemouth. A total of 3 of these cases reported having visited the public gardens and/or Bournemouth beach in their exposure histories.

Microbiological investigation:

Case finding - The outbreak strain cultures were serotyped as EHEC O55:H7, tested positive for the presence of eae (intimin), had a stx subtype profile that was stx2a only and appeared as non-sorbitol fermenting colonies on SMAC but failed to grow on CTSMAC. Only one case (Case 26, who was not associated with any epidemiological cluster) was identified from the extended screening of 4200 bloody diarrhea specimens. Clearance for most cases was between 7 and 84 days (mean: 43 days) however EHEC O55:H7 continued to be detected in the feces of an asymptomatic 7-year old case for 10 months.

Whole genome sequencing - All Dorset isolates from 24 cases and 2 cats were similar to each other forming a distinct clade within 5 SNP differences of the outbreak strain of EHEC O55:H7. They were very similar (1-12 SNPs) to 6 Irish isolates (5 were within 5 SNPs) from 2013 to 2014 but relatively distant (over 250 SNPs) from the 5 earlier Irish isolates. Isolates linked to the nursery were more closely related to each other than to isolates from the earlier cases in 2014 (Figure 2). Despite a period of almost 4 weeks between symptomatic cases in the nursery, phylogenetic analysis showed the isolates from 3 cases from weeks 47 and 48 in 2014 were identical to the isolate from the case identified in week 43, consistent with human-to-human transmission. Case 1 and the primary nursery case (Case 5) were diagnosed by serology therefore no isolate was available for sequencing.

International investigations:

Other EHEC O55 isolates - All Irish cases were living in counties along the east coast and there were no common exposures between previous Irish cases occurring during 2012-14. There were no epidemiological links between the Dorset cases and the Irish cases. With the exception of the isolates from ROI, other EHEC O55 isolates reported elsewhere in Europe in 2014 had different microbiological characteristics than the Dorset cluster (different serotype, stx profile and ability to ferment sorbitol) thus were not included in this investigation. There were 3 _E. coli_ O55 cases elsewhere in England reported during the period of the outbreak who did not meet the outbreak case definition. One was EHEC O55:H9 stx2d, another was a returning traveler who had positive serology only for _E. coli_ O55 and therefore the strain could not be identified whilst the 3rd case was EHEC O55:H7 but was 10 SNPs apart from the outbreak WGS cluster and had no epidemiological link to Dorset.

Animal movement - Bird populations remained constant in the south west and south east England from 2013 to 2015, suggesting no new risks. Teal and black-headed gulls were the only species identified where there was significant level of movement between ROI, south England and Europe. Black headed gulls are common in Great Britain and there are large colonies along the south and east coasts of England.

A total of 1149 cattle from ROI were moved to 69 separate premises in Dorset in the 2 year period between 2013 and 2014. These premises are located mainly in the north and west of the county, away from, but upstream of, the residences of (co)primary cases in the south of the county near the coast (Figure 3).

Control measures and communication
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We managed cases and contacts using national EHEC guidance (18), including appropriate exclusion from work, school or childcare of confirmed cases and contacts at increased risk of transmission, until shown microbiologically to have cleared the infection (18). We provided advice on hand and food hygiene together with guidance on environmental cleaning and disinfection to cases and contacts and to venues such as a petting farm, nursery and schools. Staff and children were screened at the nursery; a measure that is not in the national guidance but has been used in other outbreaks (23). In total, 8 children were excluded for a period of time ranging from 7 to 84 days until microbiological clearance.

The nursery with the cluster of cases closed voluntarily on [26 Nov 2014] to facilitate screening of staff and children and deep cleaning of the premises.

Proactive public messages initially focused on basic infection control measures but became more specific, advising people to be extra vigilant with hand hygiene before preparing food and after contact with pets and animals. In response to widespread media interest, including coverage criticising PHE's handling of the outbreak, the regional BBC Health Correspondent was offered a full access briefing including a visit to PHE laboratories. This resulted in factually accurate reporting and reiteration of the public health messages in a BBC television documentary in November 2015, with content promoted on its Facebook page (24).

Discussion
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In addition to being the first recorded outbreak of EHEC O55:H7 in England, striking features of the outbreak include its seasonality, the high proportion of cases developing HUS (13/31) compared with the background rate for EHEC O157 (5 percent) (2) and the geographical component linking all (co)primary cases to Bournemouth and Weymouth in Dorset. Evidence of human-to-human transmission of EHEC O55:H7 within the nursery cluster was shown by the propagated epidemic curve and WGS with cases in this cluster forming a largely homogenous monophyletic sub-cluster among isolates in the outbreak as a whole. Overall, isolates showed more diversity than would be expected in a STEC point-source outbreak (25). The genetic similarity between isolates taken from Dorset cases and the 2013-14 Irish cases suggests infection by the same or closely related populations of EHEC O55:H7 and may represent a common zoonotic reservoir. Enhanced surveillance suggested infection to be less widespread than feared in the Dorset population. Contacts were tested more widely than normal (for a EHEC outbreak) using culture/PCR and/or serology ensuring the identification of asymptomatic household contacts. To date there have been no further cases in this WGS cluster, although other _E. coli_ O55 cases have occurred elsewhere in England. Despite the use of an iterative re-interviewing process, no common exposures linked all primary cases and food, water and environmental testing was negative for contamination by EHEC O55:H7. There was little evidence to support the hypotheses of contaminated food items or drinking water or a specific recreational/environmental exposure. Given this, and the geographical clustering around 2 areas of Dorset, the 3rd hypothesis of a local endemic zoonotic infection acquired in humans from infected pets and/or directly from the environment seems the most likely cause of this outbreak.

Due to the protracted nature of the outbreak, problems in recall may have hampered the effectiveness of the iterative re-interviewing approach, given the time lag between cases. It is possible that using the onset date of the associated primary case as the starting point for a 14-day exposure history-taking among asymptomatic cases missed important exposures if their infection had been acquired earlier. However, all of the asymptomatic cases were picked up through screening of contacts or nursery screening, all those identified by serology were epidemiologically linked to a WGS-confirmed case and many asymptomatic cases were adult household contacts of children, so it is likely that the majority of them were 2ary cases whose infection was acquired by human-to-human transmission. Even if putative exposures had been identified, having only 10 (co)primary cases would have made hypothesis testing via an analytical study challenging.

The environmental hypothesis appears most likely although there were no positive environmental samples (including boot socks, animal feces, bird sanctuaries or water) to confirm it. The delay between symptom onset and environmental sampling could have reduced the chance of a positive finding and sensitivity of direct culturing from feces can be poor if EHEC numbers are low. Similar delays may also have reduced the likelihood of finding a positive sample among pets. There is currently no evidence of EHEC O55:H7 in the cattle population in the UK but cattle and other ruminants are a known source of EHEC (26). Delays between infection and sampling, particularly among screened contacts, may also have led to cases being missed early in the outbreak. However, after the 1st few cases we tested contacts more widely than normal for a EHEC outbreak and detected a number of asymptomatic household contacts using serology, so we are confident that any symptomatic contacts would also have been identified microbiologically, either via culture or serology. Furthermore, it is possible that asymptomatic or mild diarrheal illness may have been underestimated as most case ascertainment of EHEC O55:H7 was due to presentation with HUS, with non-HUS-associated infections being missed apart from the periods of enhanced surveillance. The absence of additional cases arising from the testing of all diarrheal specimens from local and regional laboratories for EHEC O55:H7 over a 12-week period is evidence against this, however, this extended testing regime occurred in the autumn, when fewer or no cases were expected.

EHEC O55:H7 is phylogenetically closely related to EHEC O157:H7 (12,25) and assumed therefore to have similar exposure risks and transmission routes. The observed seasonality (July-October 2014; May-September 2015) is similar to that seen for EHEC O157 (April-September) in England and Wales (27). This may reflect greater time spent outdoors during warmer months of the year, increasing exposure to the environment. Migratory birds as a transmission source common to Dorset and ROI could also help explain both the seasonality and genetic similarity between Irish and Dorset cases and birds (rooks) have previously been linked to EHEC O157 infection in children (28). The analysis focused on bird migration between ROI and Dorset but it is also possible that EHEC O55:H7 was introduced by migratory bird species, with a shared winter feeding ground, that use the coast of ROI and the coast of England as destinations for summer feeding. In 5 of the 6 primary cases linked to Bournemouth, symptom onset occurred in a period of 1-9 days following flooding events, suggesting these events could have played a role. 3 of these 4 cases reported visiting the public gardens or beach in Bournemouth and their illness could plausibly be explained by exposure to land recently flooded by stream water contaminated by animal feces or to the sea into which the stream discharges. The EHEC O55:H7 positive fecal specimens from 2 cats provided evidence that domestic pets may act as a vector for the pathogen and may support a hypothesis of an environmental or local zoonotic reservoir. This is consistent with reports of EHEC O145 serotypes in sporadic HUS in children which were also isolated from their asymptomatic pet cats (29,30). There were no common factors found for foods consumed by the pets, but it was not possible from the information collected to determine the extent to which cases' pets interacted with the rural environment, wildlife or rodents. It is possible that there are several vectors responsible for the environmental spread and cases could also have acquired EHEC O55:H7 directly from the environment.

This outbreak provides a number of learning points. Proactive media engagement was important and helped to ensure risk communication throughout the outbreak was effective and that the timing and control of information could be maintained by PHE. The evidence from WGS of isolates forming a closely related cluster was an important driver behind the extensive investigations undertaken. As WGS is used increasingly in England for outbreak investigation and detection, it is likely to be a driver in the future for investigating small outbreaks of illness that are not clearly linked epidemiologically (31,32).

The introduction of an additional SMAC agar plate into local laboratory processes helped reduce the number of cultures being sent to GBRU and enabled local detection of likely EHEC O55:H7 in the absence of PCR. Enhanced surveillance through local laboratories, WGS, boot sock sampling and the combined use of hydrological and cattle census data are all methods that could be adapted and applied when investigating outbreaks of emerging pathogens with unclear etiology. We conclude that although the cause of this outbreak remains elusive the varied investigations helped narrow the focus to a dispersed environmental source and/or a zoonotic reservoir.

References [available at original URL. - Mod.LL]

[Authors: McFarland N, Bundle N, Jenkins C, et al]

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Communicated by: ProMED-mail <promed@promedmail.org>

[ProMED reported on this "smoldering" outbreak of EHEC O55 when it was occurring in 2014-2015. This well-done report summarizes what was found out about the outbreak and speculates on the epidemiology. It is interesting that a higher percentage of HUS occurred in the cohort of cases and that similar strains had been found in Ireland previously.

As a reminder, other non-O157 _E. coli_ serogroups that have been associated with EHEC disease include motile ones such as O26:H11 and O104:H21 and non-motile ones such as O111:NM (or H-). Such non-O157 isolates can be obtained from sheep and cattle, and although they cause as many as 30 per cent of outbreaks of VTEC (1), they appear to be somewhat less (or at least more variably) virulent in a variety of in vivo and in vitro assays (2-4). In analyzing the genetic and phenotypic profiles of non-O157 groups, it has been found that they belong to their own lineages and have unique profiles of virulence traits different from O157 (5). The serogroups appearing to be most prominent are O26, O111, O128, and O103 (6), the former serotype being the implicated strain in this outbreak.

If a laboratory is using sorbitol-MacConkey (sMAC) plates to identify EHEC by virtue of O157's inability to ferment sorbitol, the non-O157 strains will be missed. In a 3-year pediatric study from the University of Washington, USA (7), 1851 stool samples were processed for sorbitol fermentation as well as toxin production by EIA (enzyme immunoassay), and 28 strains of O157 were found along with O103 (4 strains), O118 (2 strains), O111 (2 strains), and 3 other strains.

References:
1. Hussain HS and Omaye ST. Introduction to the food safety concerns of verotoxin-producing _Escherichia coli_. Exp Biol Med. 2003; 228(4): 331-2. Abstract available at: <https://www.ncbi.nlm.nih.gov/pubmed/?term=12671175>.
2. Blanco J, Blanco M, Blanco JE, et al. Verotoxin-producing _Escherichia coli_ in Spain: prevalence, serotypes, and virulence genes of O157:H7 and non-O157 VTEC in ruminants, raw beef products, and humans. Exp Biol Med. 2003; 228(4): 345-51. Abstract available at: <https://www.ncbi.nlm.nih.gov/pubmed/12671177>.
3. Law D and Kelly J. Use of heme and hemoglobin by _Escherichia coli_ O157 and other Shiga-toxin-producing _E. coli_ serogroups. Infect Immun. 1995; 63(2): 700-2. Available at: <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC173054/>.
4. Tzipori S, Wachsmuth KI, Smithers J and Jackson C. Studies in gnotobiotic piglets on non-O157:H7 _Escherichia coli_ serotypes isolated from patients with hemorrhagic colitis. Gastroenterology 1988; 94 (3): 590-7. Abstract available at: <https://www.ncbi.nlm.nih.gov/pubmed/?term=3276573>.
5. Schmidt H, Geitz C, Tarr PI, et al. Non-O157:H7 pathogenic Shiga-toxin producing _Escherichia coli_: phenotypic and genetic profiling of virulence traits and evidence for clonality. J Infect Dis. 1999; 179(1): 115-23. Available at: <https://academic.oup.com/jid/article-lookup/doi/10.1086/314537>.
6. Bettelheim KA. Role of non-O157 VTEC. Symp Ser Soc Appl Microbiol. 2000; (29): 38-50S. Abstract available at: <https://www.ncbi.nlm.nih.gov/pubmed/10880178>.
7. Klein EJ, Stapp JR, Calusen CR, et al. Shiga toxin-producing _Escherichia coli_ in children with diarrhea: a prospective point-of-care study. J Pediatr. 2002; 141(2): 172-7. Abstract available at: <https://www.ncbi.nlm.nih.gov/pubmed/?term=12183710>.
- Mod.LL

A HealthMap/ProMED-mail map can be accessed at: <http://healthmap.org/promed/p/279>.]

[See Also:
E. coli EHEC - UK (02): (Scotland) O157, race participants, alert: http://promedmail.org/post/20170705.5152938
E. coli EHEC - UK: (England) O157: http://promedmail.org/post/20170622.5123423
2016
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E. coli EHEC - UK (09): (Scotland) O157, unpast cheese, children, fatal http://promedmail.org/post/20160916.4493645
E. coli EHEC - UK (08): (Scotland, England) O157, unpast cheese, recall, fatal http://promedmail.org/post/20160914.4488415
E. coli EHEC - UK (07): (Scotland, England) O157, unpast. cheese, fatality http://promedmail.org/post/20160907.4469162
E. coli EHEC - UK (06): (Scotland, England) O157, unpast. cheese, alert, recall http://promedmail.org/post/20160817.4420279
E. coli EHEC - UK (05): (Scotland, England) O157, unpast. cheese, alert, recall http://promedmail.org/post/20160729.4379645
E. coli EHEC - UK (04): O157, salad, fatalities http://promedmail.org/post/20160725.4367897
E. coli EHEC - UK (03): (England) O157, salad, fatalities http://promedmail.org/post/20160715.4347888
E. coli EHEC - UK (02): (England) ex Egypt http://promedmail.org/post/20160707.4330782
E. coli EHEC - UK: O157, possible salad link, RFI http://promedmail.org/post/20160706.4328712
2015
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E. coli EHEC - UK (07): (Scotland) O157, venison http://promedmail.org/post/20151019.3726963
E. coli EHEC - UK (06): (England) O55 http://promedmail.org/post/20150923.3655007
E. coli EHEC - UK (05): (England) O157, precooked meat products http://promedmail.org/post/20150726.3537630
E. coli EHEC - UK (04): (England) O157, precooked meat products http://promedmail.org/post/20150718.3520087
E. coli EHEC - UK (03): (England) O55 http://promedmail.org/post/20150528.3392716
E. coli EHEC - UK (02): (England) nursery school, O157 http://promedmail.org/post/20150506.3345725
E. coli EHEC - UK: (England) O55 http://promedmail.org/post/20150211.3160384
2014
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E. coli EHEC - UK (20): (England) O55 http://promedmail.org/post/20141225.3053978
E. coli EHEC - UK (19): (England) O55 http://promedmail.org/post/20141210.3025667
E. coli EHEC - UK (18): (England) O55, nursery school http://promedmail.org/post/20141129.2999769v
E. coli EHEC - UK (17): (England) O55, nursery school link http://promedmail.org/post/20141126.2992343]

Published 27-09-2017 in Focus on , last update 27-09-2017

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