Travel Health

You are in: Skip Navigation LinksHPS Home | Travel Health | Weekly Report Item

Weekly Report Articles

05 January 2006

VTEC in Scotland 2004: Enhanced surveillance and reference laboratory data


Scotland continues to report higher rates of infection with verotoxigenic Escherichia coli serogroup O157 (VTEC O157) than elsewhere in the UK1 (Figure 1). Background incidence has been around 200 to 250 cases per annum in recent years, although numbers were unusually low in 2003. Infection with E.coli O157 has been linked to serious health outcomes such as haemolytic uraemic syndrome (HUS)2, particularly in childhood renal failure3. Thrombotic thrombocytopaenic purpura (TTP), involving neurological complications, was linked to fatalities in the central Scotland outbreak of 1996/19974. Although foodborne transmission accounted for the two largest outbreaks in Scotland5,6, most cases are sporadic. Exposure to farm animal faeces is the main risk factor for sporadic E.coli O157 infections in Scotland7, and some outbreaks in recent years have involved campsites or water supplies contaminated by farm animal faeces8,9. Secondary transmission can occur via person-to-person spread, with asymptomatic infection presenting a further, hidden risk.

Most isolates of E.coli serogroup O157 are verotoxigenic i.e. the organisms possess genes for the production of verotoxin (vtx) capable of causing disease in humans. Possession of vtx genes is more varied amongst other serogroups of E.coli. Non-O157 VTEC has been strongly associated with HUS in some other European countries. In recent years, small but increasing numbers of non-O157 VTEC have been reported in Scotland10, possibly as a result of E.coli O157 Task Force recommendations.

Health Protection Scotland (HPS) established population-based enhanced surveillance of E.coli O157 in 1999, to identify trends and changes in the epidemiology and outcome of infection on a national scale. HPS liaises closely with the Scottish E.coli O157 Reference Laboratory (SERL) and with public health teams throughout Scotland. Enhanced surveillance includes factors not identifiable from routine surveillance (e.g. secondary and asymptomatic cases, and hospital admissions). Sporadic and outbreak cases can be differentiated and compared. Infections with non-O157 VTEC are also now included in HPS enhanced surveillance. VTEC-related cases of HUS and TTP reported to public health by clinicians were not identified at national level until 1999 when VTEC enhanced surveillance began11. Additional direct clinical reporting to HPS of HUS, TTP and other thrombotic microangiopathies, irrespective of causation, was established in 200312.

As part of the public health network in Scotland, enhanced surveillance can provide real-time information to assist risk assessment, risk management and policy development, both locally and nationally. VTEC surveillance reports are also circulated to participating patients and physicians; to public health practitioners, microbiologists, Scottish Executive13, the Food Standards Agency (Scotland)14 and other relevant agencies. Enhanced surveillance also provides information for UK15 and European16 health protection initiatives, and links data with the Health Protection Agency17, for UK-wide comparisons.


A case is defined as a person-infection-episode, with microbiological confirmation of infection, identified from isolates cultured from faeces, or from detection of antibodies to E.coli O157 in serum, or both. HPS receives reports of culture positive cases of E.coli O157 from SERL and from diagnostic laboratories throughout Scotland. SERL receives clinical samples (isolates, faeces and sera) from diagnostic laboratories. Using a series of phenotypic and genotypic tests, SERL confirms the presence of E.coli O157 in these samples, and reports any additional cases to HPS, including seropositives. Cases of non-O157 serogroups of VTEC are reported by SERL, and by those diagnostic laboratories currently screening for these organisms. SERL subsequently types all isolated organisms using phage typing and pulsed-field gel electrophoresis (PFGE).

HPS integrates data from SERL and diagnostic laboratories with information collected from public health teams in NHS boards. A standardised minimum dataset is compiled for each case, including exposures and clinical outcomes such as hospital admissions (of at least one overnight stay). Patients with HUS are identified from clinician or GP reports, either via public health or direct to HPS. Asymptomatic infections are identified. Sporadic cases are differentiated from cases linked to general outbreaks i.e. incidents involving members of more than one household, or institutions. Patients living within the same household are defined as household sporadic cases. Exposures to potential risk factors are checked for all cases. Ethical approval was obtained for any direct contact with patients and physicians, from the Multi-centre Research Ethics Committee (MREC) for Scotland. VTEC enhanced surveillance links with other HPS systems, to maximise the information on health risks that can be derived from publicly-funded surveillance. ENSHURE12 facilitates additional clinical reporting of thrombotic microangiopathies, irrespective of microbiological confirmation, to identify the proportion of all HUS or TTP cases associated with E.coli O157 infection. ObSurv18 covers general outbreaks of all infectious intestinal diseases (IID) in Scotland, including those identified during VTEC surveillance. Any significant exposures revealed during VTEC surveillance (e.g. visits to an open farm in another area) are reported in real time to the relevant public health team. Cases believed to have acquired infection outwith Scotland are reported to the relevant international health authorities.

This annual report analyses the minimum datasets for all E.coli O157 infections reported to HPS in 2004. The results of continuing long-term research, investigating whether patients experience health effects over time, will be published at a later date.


1 Enhanced surveillance of culture and serum positive cases of E.coli O157

1.1 Total number of E.coli O157 infections reported to HPS in 2004

The HPS enhanced surveillance project includes all laboratory confirmed cases of E.coli O157 infection. In 2004, a total of 210 cases were reported to HPS, of which 209 were culture positive; one further case being confirmed by serodiagnosis alone (Table 1).

This total of 210 culture or serum positive cases represented an increase of 37%, compared to 153 cases reported in 2003. The rate per 100,000 population was 4.1 cases in 2004, compared to 3.0 in 2003. In 2003, case numbers had decreased by 34%, compared to 200210. Despite the subsequent increase in 2004, the year-end total for both culture and serum positive cases was still lower than in 2002 (231 cases) and 2001 (243 cases). Thirteen of the 210 cases in Scotland were identified due to forwarding of samples to SERL, in line with Task Force recommendations for further laboratory testing when clinical diagnosis of E.coli O157 cannot be confirmed locally. Confirmation of infection can have implications for clinical management of the patients concerned, and for infection control measures.

1.2 Geographical distribution and rates per 100,000 population

As in previous years, case numbers and rates were highest in Grampian NHS area, given that island health board rates can be artificially increased due to small population figures (Table 2 and Figure 2). The next highest mainland rates occurred in Dumfries and Galloway. Whilst Fife reported the third highest rate, eight of the 22 cases probably acquired infection in an outbreak originating outwith Scotland. Although the national rate increased in 2004, rates in some areas changed little or decreased. Western Isles and Shetland reported no cases.

1.3 Date of infection

The only time indicator for all cases provided by routine surveillance, is report week, which is subject to delays. Enhanced surveillance enables more precise timing i.e. onset of symptoms, or date of first positive specimen for asymptomatic cases. Most infections in 2004 occurred in the middle months of the year (Figure 3). Whilst case numbers at the 2004 year end were 37% higher than 2003, this increase was not consistent across the year. At the end of April 2004, case numbers were actually 33% lower than 2003. By the end of September, numbers were 43% higher.

1.4 Sporadic or outbreak cases

Of the 210 cases, 39 (19%) were reported by local public health teams to be part of outbreaks (Table 3). The majority of cases were apparently sporadic infections, as has been the case in previous years.

The 39 outbreak cases were associated with 11 outbreaks. Six of these outbreaks were identified during enhanced surveillance follow-up, without which the 25 cases involved might have appeared to be sporadic infections. Nine of the 11 outbreaks were reported as having their source of infection in Scotland; one appeared to have originated in England with person-to-person spread in Scotland; and one involved two otherwise unconnected cases who visited the same area of Italy, and whose isolates had the same unusual phage type.

In seven of the 11 outbreaks, involving 25 (64%) of the 39 outbreak cases, local investigators reported exposure to farm animals or farm environments. Two of the seven farm-related outbreaks involved private water supplies contaminated with E.coli O157, one of which was consumed on farm premises. E.coli O157, with the same phage type and an undistinguishable PFGE profile, was identified in cattle faeces by the source of the second supply, as well as in the water itself. A third livestock-related outbreak involved burn water contaminated with E.coli O157; cattle had been at the burn. The other four outbreaks involved farm residents, farm visits, contact with farm animals (including horses), or with areas contaminated by their faeces; no other significant risk factors were identified in these outbreaks. Nineteen of the 25 cases in farm-related outbreaks were children.

A specific source of infection was reported in only one of the other four outbreaks, where occupational contact with butcher meat was suspected as one of the means of transmission, but not confirmed microbiologically. Six of the 14 case in non-farm related outbreaks were children. (Details of all outbreaks of infectious intestinal disease in 2004 were published in HPS Weekly Report, 2005/5018).

1.5 Symptomatic or asymptomatic cases

Whilst most patients with E.coli O157 experienced illness, 20 (10%) of the 210 cases reported no symptoms that would have indicated E.coli infection (Table 4). Seven (35%) of the 20 asymptomatic patients were children under 16. Most asymptomatic patients (13/20, 65%) were not linked to outbreaks, but to other sporadic positive cases in the same household. Asymptomatic patients may not necessarily acquire infection from others: 16 of the 20 cases in 2004 had themselves been exposed to risk factors (e.g. visiting premises, or drinking water, contaminated by farm animal faeces).

Bloody diarrhoea was reported for 130 patients (62%). A further 39 patients (19%) had diarrhoea with no reported blood. Abdominal pain, accompanying diarrhoea or bloody diarrhoea, was reported by 96 patients (46%). Only two patients had abdominal pain as their sole reported symptom. Nineteen patients (9%) were reported with diarrhoea, but whether they also had bloody diarrhoea was unknown.

1.6 Person-to-person transmission

Local investigators reported that 12 (6%) of the 190 symptomatic patients in 2004 were likely to have acquired infection from person-to-person, or secondary, transmission (Table 5). First-hand exposure to potential risk factors was identified for the other 178 cases. There was a statistically significant reduction in the proportion of secondary cases in 2004, compared with 13% secondary cases in 2003 (X2 = 4.60, df 1, P = 0.03). Six of the 12 secondary cases in 2004 were not part of outbreaks, but were linked to other cases within the same household. Half of all secondary cases were children under 16 years.

1.7 Age and gender

Ages ranged from 4 months to 91 years. The mean age was 27 years, the median 19 years. The most frequently reported age was 2 years (18 cases, 9% of all cases). Higher rates of infection occurred amongst young people (Figure 4). Children under 16 years accounted for almost half (48%) of all cases, with the under 10s accounting for 38% of all cases. An age of 65 years or over was reported in 10% of cases.

The overall rise in rates of infection in 2004 was reflected in most age groups. Rates for children aged 5 to 9, which had fallen sharply in 2003, rose markedly. Rates for ages 15-19 remained virtually unchanged, as has been the case over the last four years. The only drop in rates was amongst ages 20-24, which was the only age group to show an increase in 200310.

Females were in the majority overall, with 110 out of 210 cases (52%). A Mann-Whitney test showed that ages of males and females were similar (P = 0.295).

1.8 Admissions to hospital

Hospital admission for at least one night was required by 91 (43%) of the 210 patients reported in 2004. This was the second highest proportion admitted since 1999, the average for the six year period being 40% admitted each year. Given that patients were symptomatic, in 2004 the proportion of sporadic cases hospitalised (48%) was comparable with outbreak cases (44%) (X2 = 0.20, df 1, P = 0.65). Only 16% of the 91 admissions with E.coli O157 infection in 2004 were related to outbreaks. Hospitalisation was less common amongst secondary cases (33%), compared to primary cases (48%) but this difference was not statistically significant (X2 = 1.01, df = 1, P = 0.31).

1.9 Progression of illness to HUS or TTP

Twenty-two (11%) of the 210 patients with E.coli O157 infection in 2004 developed HUS, compared to 12% in 200310. All but three of the 22 patients with HUS in 2004 were under 16 years old, and 12 of the 22 (55%) were children under 5.

Over 70% of all patients with HUS were sporadic cases, not linked to any known outbreak. The proportion of all sporadic cases developing HUS (10%) was similar to that of outbreak cases (13%) (Fisher’s exact test, P=0.57). Amongst patients who acquired infection by secondary, person-to-person transmission, the proportion developing HUS (8%) was similar to the proportion amongst primary cases (12%) (Fisher’s exact test, P=1.0).

One of the 22 cases of HUS in 2004 would not have been identified without direct clinical reporting via ENSHURE12, as the local public health team had not been informed of the clinical outcome for this particular patient. In another patient with E.coli O157 infection, HUS was not identified by public health or clinical reporting, but was identified when the family completed a follow-up questionnaire for VTEC enhanced surveillance.

1.10 E.coli O157 infection and HUS in residents of other countries who visited Scotland

Two additional cases of E.coli O157 infection with HUS, in children from other UK countries who visited Scotland, were reported to VTEC enhanced surveillance during 2004. The connection to Scotland in these cases would otherwise not have been identified because laboratory confirmation and clinical diagnosis took place in other countries. Both children had been exposed to risk factors in Scotland, and were reported to HPS by the public health teams of the areas visited. One of these children was part of one of the farm-related outbreaks linked to contaminated private water supplies. The other had livestock-related exposures.

In addition to the two children who developed HUS after visiting Scotland, VTEC surveillance received reports of another four residents of other UK countries who were identified with E.coli O157 infection after returning from Scotland. These patients had also been exposed to risk factors in Scotland.

1.11 Deaths

Two deaths in patients with E.coli O157 infection were reported in 2004. Both patients died from conditions not necessarily related to infection. Neither patient was reported with HUS or TTP. Information on whether E.coli O157 contributed in any way to their deaths was not available to HPS. Both patients were aged over 50, and were reported to have had sporadic infections, not connected to any outbreak. No significant exposures were identified for either patient.

1.12 Imported infections and co-morbidity

Based on dates of travel, any known exposures to risk factors, and onset, 24 cases (11%) were reported by local investigators to have acquired infection outwith the UK. Only 2% would have been identified as imported infections, by routine surveillance alone. Co-infection was reported in six (3%) of the 210 patients in 2004.

1.13 Exposures to potential risk factors for E.coli O157 infection

Various livestock-related exposures were reported for 116 (55%) of the 210 cases in 2004, of whom 69 (33% of all cases) had more than one such exposure. Livestock-related exposures were more common amongst children under 16 (72%) compared to patients aged 16 and over (40%) (X2 = 21.69, df 1, P < 0.0005). Regular livestock-related exposures were reported for 48 of these 116 individuals (23% of all cases, 41% of cases with livestock-related exposures) who lived on or immediately next to farms or farmland, or worked in farms, stables etc. A higher proportion of patients with regular livestock-related exposures developed HUS (19%), compared to those with irregular/one-off exposures (9% with HUS) or those with no such exposures (7%). Perhaps reflecting the numerically small total of HUS cases (22 patients), this difference did not reach statistical significance at the 5% level (X2 = 4.62, df 2, P = 0.099).

Visits to farm or livestock premises with grazing animals (that were not the patient’s residence or workplace) were reported for 58 cases (28% of all cases, 50% of cases with livestock-related exposures). These premises included private or visitor farms, country parks, stables, livestock markets and shows.

Contact with farm or grazing animals, or exposure to their faeces, was reported in 53 cases (25% of all cases, 46% of those with livestock-related exposures); 27 of these 53 having regular exposure. Some animal/faecal contact did not result from actually going onto farm premises, but involved reaching into fields to feed or pet cows, horses, etc. For seven cases (3% of all cases, 6% of livestock-related cases), the only identifiable risk factor of any kind was being in a rural environment, not on farm premises but with potential for contact with grazing animals or their faeces (e.g. visiting holiday accommodation immediately next to pasture). Contact with poultry or birds was not counted as a livestock-related exposure, and was reported for only one of the 210 cases in 2004.

Nine of the 116 cases with livestock-related exposures were linked to four private domestic water supplies on farm land or premises. All four supplies were positive for E.coli O157 and failed local authority water tests. Cows had grazed around the source of three supplies, and E.coli O157 was identified in cattle faeces at one source. The fourth positive supply was on farm premises. HUS was reported in two children amongst these nine cases; another two cases had not drunk the water themselves but were reported as infections due to secondary spread. Another eleven livestock-related exposures were linked to private water supplies, which failed with E.coli present, suggesting contamination had occurred. Whilst E.coli O157 was not identified in any of these supplies, not all the water samples may have been specifically tested for this serogroup. Nine of these patients with failed private water had supplies which were on farm land or premises; these patients themselves also lived on, next to, or worked on farms i.e. the water supply was not their only livestock-related exposure. The location of supply for the other two patients was unknown, but the patients themselves had animal contacts. Two further livestock-related cases drank water from a burn from which E.coli O157 was isolated; cattle having been seen at the burn.

For 34 (16%) of the 210 cases, local investigators reported food-related risks (e.g. consuming food from barbeques or other temporary facilities). However, only one of these patients specifically reported eating undercooked food, and E.coli O157 was not identified in any foodstuffs linked to these cases. Eleven of these 34 patients also had livestock-related exposures, that local investigators judged the more likely source of infection. For another 11, the food-related exposures occurred abroad, and included eating salads washed in, or drinking, local tap water; eating food prepared on boats, coaches, campsites or barbeques; or eating burgers (five patients). Of the remaining 12 patients with food-related exposures, but no travel or livestock-related risk factors, two consumed burgers from mobile outlets; four ate barbeque food; three had substantial raw meat contact; and three had close contacts working with raw meat. Five patients in 2004 had contact with untreated water as their only identified risk factor, three of them outside the UK. No livestock was reported around the waters involved.

For 64 (31%) of the 210 cases in 2004, no livestock-related, water or significant food exposures were reported to HPS. Seven of these cases were imported infections, in patients for whom travel outwith the UK was the only identifiable risk factor. Another six had infection due to secondary transmission, one from a patient with a farm exposure, the other five from patients who had no identified exposures themselves. Three of these 64 patients developed HUS.

2 Reference laboratory results

Isolates from 208 of the 209 culture positive cases reported to HPS were available for further microbiological investigation at SERL. The remaining culture positive case was reported to HPS by a diagnostic laboratory, but no isolate was forwarded to SERL.

SERL received 2336 clinical samples in 2004, from 12 of the 15 NHS board areas, compared with 1578 samples received in 2003. Of these 2336 samples, 257 (11%) tested positive for E.coli O157, resulting in the 209/210 cases that were either identified or confirmed by SERL (208 culture positive and one seropositive, some with multiple samples). Of the total 2336 clinical samples, 2021 were faecal samples forwarded to SERL in line with E.coli Task Force recommendations1, from patients with symptoms indicative of infection, but no local laboratory confirmation. From these samples, 13 of the total 210 cases of E.coli O157 infection were identified, that might not have been detected by routine laboratory methods.

Of the 208 isolates of E.coli O157 available for further investigation at SERL, 206 (99%) were verotoxigenic. Although the majority possessed the verotoxin 2 (vtx2) gene only, 29 isolates (14%) possessed both verotoxin 1 (vtx1) and verotoxin 2 (vtx2 ) genes (Table 6). All of the 21 patients with HUS who were culture positive (the 22nd patient with HUS was seropositive only) had isolates that possessed the vtx2 gene only.

Amongst the 206 isolates possessing any verotoxin genes, the proportion possessing vtx2 gene only decreased in 2004 (86%) compared to 2003 (93%) (X2 = 4.36, df 1, P = 0.04). Of the two non-verotoxigenic isolates in 2004, one had PT14, and was from a patient reported to have acquired infection abroad, who had co-infection with Shigella sonnei. The other non-verotoxigenic isolate had phage type RDNC, and was from a patient with bloody diarrhoea with no co-infection or travel history. This was also the only E.coli O157 isolate examined by SERL in 2004 that did not possess the E.coli attaching and effacing gene (eae), which is responsible for the intimate attachment of the E.coli cell to the epithelial lining of the intestine, and may be an indicator of human pathogenic potential19.

SERL identified phage type (PT) 21/28 in 58% of available isolates (Table 7). Although PT21/28 remained predominant, as has been the case in Scotland since 1998, this was the lowest proportion of cases accounted for by PT21/28 since enhanced surveillance began in 1999. From 1999 to 2003, PT21/28 accounted on average for 65% of cases per annum. PT2 was next most frequently identified type in 2004, followed by PT8 and PT32. In 2%, isolates were identified as having an RDNC phage type, where the phages react but do not conform to a known pattern. Eleven different phage types were identified in 2004, compared to twelve in 2003.

The proportions accounted for by other phage types also varied compared to previous years, and the increase of 37% in annual figures in 2004 was not consistent across all phage types. Figures for PT2 were the highest since 1997, and were 169% higher than in 2003 (13 cases with PT2). Reports of PT8, whilst not as high as in some previous years, also rose by 167% compared to 2003, when only nine isolates with PT8 were identified. There were no reports of PT4 in 2004, although figures for PT4 in 2003 had been the highest since 1999.

All 121 cases with PT21/28, and most cases with other PTs, possessed vtx2 only (Table 8). PT8 was markedly different, with all cases having isolates that possessed both vtx1 and vtx2. Amongst PT14 isolates, toxin distribution was more varied, although numbers were small. Isolates with both vtx1 and vtx2 accounted for a higher proportion of forwarded isolates in 2004, compared to 2003 (7%), perhaps reflecting the higher proportion of PT8 isolates in 2004.

Amongst the 185 UK-acquired cases for whom PTs were available, livestock-related exposures were more common in cases with PT21/28 (70%) or PT2 (53%), than in cases with other phage types (31%) (X2 = 16.4, df 2, P < 0.0005). Food-related exposures were more common in cases with PT2 (15%), compared to PT21/28 (5%) or other phage types (3%) but the small numbers for food and other non-livestock related exposures precluded further statistical analysis.

3 Non-O157 VTEC

3.1 Laboratory reported isolations of non-O157 E.coli in 2004

A further 95 isolates of non-O157 E.coli were reported to HPS in 2004, within which 29 different serogroups were identified (Table 9). Of the 89 non-O157 isolates either cultured at, or forwarded to SERL, seven (8%) were verotoxigenic.

3.2 HUS in patients with non-O157 VTEC

Verotoxigenic E.coli O145 was identified in one child who developed HUS in 2004. There have been only two previously reported instances of HUS in patients with non-O157 VTEC in Scotland. The first occurred in an adult with VTEC O46 in 2000. The second was in a child with VTEC O177 infection, reported in 200312.

Discussion and Conclusions

Whilst annual totals for E.coli O157 infections decreased slightly over recent years (perhaps reflecting implementation of the E.coli O157 Task Force recommendations1), there have been marked fluctuations. Although the number of E.coli O157 infections in 2004 rose by 37% compared to 2003, this followed a 34% decrease in 2003, suggesting that 2003 was an unusual year. Despite the return to more typical incidence levels in 2004, the year-end total was lower than in most recent years20.

Rates of infection in Scotland continued to differ from those in neighbouring UK countries (Figure 1). England and Wales reported 13 outbreaks in 200417, compared to 11 amongst Scotland’s smaller population. The characteristics of E.coli O157 organisms also differed, with PT21/28 identified in 29% of cases in England and Wales17, compared to 58% in Scotland. HPS continues to pursue research partnerships in order to compare geo-spatial data on E.coli O157 cases, with livestock21 and meteorological10 data, to identify whether these factors might influence human incidence, or account for differences within the UK.

Enhanced surveillance describes the epidemiology of infection in Scotland more fully than routine surveillance, which does not for instance identify outbreaks, hospitalisations, or secondary cases. Whilst overall numbers rose in 2004, the proportion of secondary infections was around half that of 2003. There is nothing to suggest that this was due to reduced screening of contacts.

Further analysis of the VTEC dataset over time may identify whether there is any link between spread of infection, and the proportion of isolates possessing the vtx2 gene alone, which appears to be associated with more serious health outcomes22. On the other hand, although the proportion of isolates possessing only the vtx2 gene fell in 2004 (85%) compared to 2003 (92%), the proportion of patients developing HUS changed little (11% in 2004 compared to 12% in 2003). As in previous years, whether infections were sporadic, or linked to outbreaks, the proportions of patients with serious outcomes were similar. Acquiring infection by secondary spread did not reduce the likelihood of HUS, either.

Extending enhanced surveillance allowed better identification of risk factors in 2004. The substantial proportion of cases with livestock-related exposures suggests the need for greater public recognition of this risk factor. A quarter of all patients were in regular proximity to farms etc. due to residence or occupation. A marked proportion of these patients developed HUS. It cannot be assumed that regular exposure reduces the likelihood of serious health consequences.

Although six patients in 2004 were thought to have acquired infection due to occupational or substantial contact with raw meat (or through secondary spread related to raw meat contact), foodborne exposures were specifically reported in only a small proportion of cases overall. Additional data from enhanced surveillance in 2005 will allow analysis of these and other risk factors, for a larger number of cases. Phage type distribution, whilst reflecting the national prevalence of PT21/28, also appeared to reflect type of exposure. Testing for association of risk factor and phage type will also be more viable, with larger numbers provided by two years of exposure data.

The E.coli O157 Task Force1, and initiatives by Scottish Executive23, the Health and Safety Executive24 and the Royal Highland Educational Trust25, have highlighted measures that can minimise risk at visitor farms, particularly for children. Members of the public can also reduce risk by simple but effective measures such as hand washing after animal contact, and before eating. Previous initiatives could be extended, with particular emphasis on farming and rural communities. Households with private water supplies should also be included in awareness raising, as patients with HUS were directly linked to E.coli O157-contaminated water supplies. Surveillance output such as this annual report is offered to participants and is in the public domain via the internet, again aiming to increase public awareness of the potential sources of E.coli O157 infection.

Patients and their families, public and environmental health departments, general practitioners, clinicians and diagnostic laboratories continued to provide invaluable information to HPS and the Reference Laboratory; for instance the additional patient with HUS, identified only because the family participated in E.coli O157 follow-up.


To patients and their relatives who participated in HPS’s E.coli O157 enhanced surveillance, particular thanks. Also: Public health teams in NHS boards; general practitioners; Pam Taylor, Scottish E.coli O157 Reference Laboratory; consultant microbiologists and diagnostic laboratory staff; environmental health officers; Health Protection Agency Laboratory of Enteric Pathogens; Scottish Agricultural College. At HPS, Professor Bill Reilly; Alison Smith-Palmer, Ob-Surv Co-ordinator; Patricia Cassells, Lorna Whyte and Rachel Porteous.


  1. Scottish Executive Health Department/Food Standards Agency (Scotland). Report of the E.coli O157 Task Force. Edinburgh: The Stationery Office, July 2001.
  2. Tarr PI, Gordon CA, Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet 2005; 365: 1073-86
  3. Lynn RM, O’Brien SJ, Taylor CM, Adak GK, Chart H, Cheasty T, et al. Childhood Hemolytic Uremic Syndrome, United Kingdon and Ireland. Emerg Infect Dis 2005;11, 4: 590-6 ;
  4. Dundas S, Murphy J, Soutar RL, Jones GA, Hutchinson SJ, Todd WTA. Effectiveness of therapeutic plasma exchange in the 1996 Lanarkshire Escherichia coli O157:H7 outbreak. Lancet 1999; 354 (9187):1327-1330
  5. Roberts JA, Upton PA, Azene G. Escherichia coli O157:H7; an economic assessment of an outbreak. J Pub Health Med 2000; 22(1): 99-107.
  6. Cowden JM, Ahmed S, Donaghy M, Riley A. Epidemiological investigation of the central Scotland outbreak of Escherichia coli O157 infection, November to December 1996. Epidemiol Infect 2001;126(3):335-41.
  7. Locking ME, O’Brien SJ, Reilly WJ, Wright EM, Campbell DM, Coia JE et al. Risk factors for sporadic cases of Escherichia coli O157 infection: the importance of contact with animal excreta. Epidemiol Infect 2001; 127: 215-220
  8. Howie H, Mukerjee A, Cowden J, Leith J, Reid T. Investigation of an outbreak of Escherichia coli O157 infection caused by environmental exposure at a scout camp. Epidemiol Infect 2003; 131: 1063-1069.
  9. Licence K, Oates KR, Synge BA, Reid TMS. An outbreak of E.coli O157 infection with evidence of spread from animals to man through contamination of a private water supply. Epidemiol Infect 2001; 126: 135-138
  10. Locking M, Allison L, Rae L, Hanson M. VTEC in Scotland 2003. SCIEH Weekly Report 2004; 38 (49): 294-297.
  11. Locking ME, Reilly WJ. Improving our understanding: Enhanced surveillance of verocytotoxigenic E.coli O157 and health outcomes in Scotland. In proceedings of the Fifth International Symposium Escherichia coli. Edinburgh:2003. Abstract P-247 (p207)
  12. Pollock KGJ. Enhanced surveillance of haemolytic uraemic syndrome and other thrombotic microangiopathies (ENSHURE) in 2003-2004. HPS Weekly Report 2005; 39: 130-132.
  13. Scottish Executive Health Department. Health in Scotland 2004. Scottish Executive 2005. (p 38)
  14. Scottish Executive/Food Standards Agency. Implementing the recommendations of the Task Force on E.coli O157. Scottish Executive 2004. (paragraph 24)
  15. Department for Environment Food and Rural Affairs. Zoonoses Report, United Kingdom 2004. Defra Publications, London, 2005. (p 29)
  16. European Commission Health & Consumer Protection Directorate. Trends and sources of zoonotic agents in animals, feedingstuffs, food and man in the European Union and Norway 2003: Verotoxigenic Escherichia coli. (p236)
  17. Health Protection Agency. Vero cytotoxin-producing Escherichia coli O157: 2004. Commun Dis Rep CDR Wkly 2005; 15 (28): 9-10.
  18. Smith-Palmer A, Cowden J, Locking M. Annual report of general outbreaks of infectious intestinal disease in Scotland, 2004. HPS Weekly Report 2005; 39: 282-285. (p282)
  19. Kaper JB, Gansheroff LJ, Wachtel MR, O’Brien AD. Intimin-mediated adherence of Shiga toxin-producing Escherichia coli and attaching-and-effacing pathogens. In: Kaper JB, O’Brien AD eds. Escherichia coli O157:H7 and other Shiga toxin-producing E. coli strains. Washington: ASM Press, 1998.
  20. Health Protection Scotland. Gastro-intestinal infection surveillance data.
  21. Innocent GT, Mellor DJ, McEwen SA, Reilly WJ, Smallwood J, Locking ME et al. Spatial and temporal epidemiology of sporadic human cases of Escherichia coli O157 in Scotland, 1996-1999. Epidemiol Infect 2005; 133: 1033-41
  22. Boerlin P, McEwan SA, Boerlin-Petzold F, Wilson JB, Johnson RP, Gyles CL. Association between virulence factors of Shiga toxin-producing Escherichia coli and disease in humans. J Clin Microbiol 1999;37:497-503
  23. Scottish Executive Health Department. Shedding light on E.coli O157 – what you need to know.
  24. Health and Safety Executive. Avoiding ill health at open farms – Advice to farmers (with teachers’ supplement) 2002.
  25. Royal Highland Educational Trust. Health and safety for farm visits (risk assessment tools for farmers).
Images (click on thumbnail to view).

eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table eWeeklyReport Table

Author(s): Prepared by: M Locking, L Allison, L Rae, K Pollock and M Hanson Vol: 39 No: 51-52 Year: 2005 Page: