Background: Commitment to food safety is evidenced by high profile governmental initiatives around the globe. To measure progress towards targets, policy makers need to know the baseline from which they started. Aim: To describe the burden (mortality, morbidity, new presentations to general practice, hospital admissions, and hospital occupancy) and trends of indigenous foodborne disease (IFD) in England and Wales between 1992 and 2000. Methods: Routinely available surveillance data, special survey data, and hospital episode statistics were collated and arithmetic employed to estimate the burden and trends of IFD in England and Wales. Adjustments were made for underascertainment of disease through national surveillance and for foreign travel. The final estimates were compared with those from the USA. Results: In 1995 there were an estimated 2 365 909 cases, 21 138 hospital admissions, and 718 deaths in England and Wales due to IFD. By 2000 this had fallen to 1 338 772 cases, 20 759 hospital admissions, and 480 deaths. In terms of disease burden the most important pathogens were campylobacters, salmonellas, Clostridium perfringens, verocytotoxin producing Escherichia coli (VTEC) O157, and Listeria monocytogenes. The ratio of food related illness in the USA to IFD in England and Wales in 2000 was 57:1. Taking into account population rates, this ratio fell to 11:1 and converged when aetiology and disease severity were considered. Conclusion: Reducing IFD in England and Wales means tackling campylobacter. Lowering mortality rates however also requires better control and prevention of salmonellas, Cl perfringens, L monocytogenes, and VTEC O157.

In the period 1992–2000, the Public Health Laboratory Service Communicable Disease Surveillance Centre collected standardized epidemiologic data on 1,877 general outbreaks of Norovirus (formerly “Norwalk-like virus”) infection in England and Wales. Seventy-nine percent of general outbreaks occurred in health-care institutions, i.e., hospitals (40%) and residential-care facilities (39%). When compared with outbreaks in other settings, those in health-care institutions were unique in exhibiting a winter peak (p<0.0001); these outbreaks were also associated with significantly higher death rates and prolonged duration but were smaller in size and less likely to be foodborne. These data suggest that Norovirus infection has considerable impact on the health service and the vulnerable populations residing in institutions such as hospitals and residential homes. A distinct outbreak pattern in health-care institutions suggests a combination of host, virologic, and environmental factors that mediate these divergent epidemiologic patterns.

Preventing campylobacteriosis depends on a thorough understanding of its epidemiology. We used casecase analysis to compare cases of Campylobacter coli infection with cases of C. jejuni infection, to generate hypotheses for infection from standardized, population-based sentinel surveillance information in England and Wales. Persons with C. coli infection were more likely to have drunk bottled water than were those with C. jejuni infection and, in general, were more likely to have eaten pâté. Important differences in exposures were identified for these two Campylobacter species. Exposures that are a risk for infection for both comparison groups might not be identified or might be underestimated by case-case analysis. Similarly, the magnitude or direction of population risk cannot be assessed accurately. Nevertheless, our findings suggest that case-control studies should be conducted at the species level.

WGS has come of age as a molecular typing tool to inform national surveillance of STEC O157; it can be used in real time to provide the highest strain-level resolution for outbreak investigation. WGS allows linked cases to be identified with unprecedented specificity and sensitivity that will facilitate targeted and appropriate public health investigations.

The risk for diarrhea-associated HUS was higher for children infected with Escherichia coli O157 phage type (PT) 2 and PT21/28 than for those infected with other PTs.

Between 1 January 2009 and 31 December 2012 in England, a total of 3717 cases were reported with evidence of Shiga toxin-producing E. coli (STEC) infection, and the crude incidence of STEC infection was 1·80/100 000 person-years. Incidence was highest in children aged 1-4 years (7·63/100 000 person-years). Females had a higher incidence of STEC than males [rate ratio (RR) 1·24, P < 0·001], and white ethnic groups had a higher incidence than non-white ethnic groups (RR 1·43, P < 0·001). Progression to haemolytic uraemic syndrome (HUS) was more frequent in females and children. Non-O157 STEC strains were associated with higher hospitalization and HUS rates than O157 STEC strains. In STEC O157 cases, phage type (PT) 21/28, predominantly indigenously acquired, was also associated with more severe disease than other PTs, as were strains encoding stx2 genes. Incidence of STEC was over four times higher in people residing in rural areas than urban areas (RR 4·39, P < 0·001). Exposure to livestock and/or their faeces was reported twice as often in cases living in rural areas than urban areas (P < 0·001). Environmental/animal contact remains an important risk factor for STEC transmission and is a significant driver in the burden of sporadic STEC infection. The most commonly detected STEC serogroup in England was O157. However, a bias in testing methods results in an unquantifiable under-ascertainment of non-O157 STEC infections. Implementation of PCR-based diagnostic methods designed to detect all STEC, to address this diagnostic deficit, is therefore important.

SUMMARYThe aetiology of sporadic campylobacter infection was investigated by means of a multicentre case-control study. During the course of the study 598 cases and their controls were interviewed.Conditional logistic regressional analysis of the data collected showed that occupational exposure to raw meat (odds ratio [OR] 9 37; 95 % confidence intervals [CI] 2 03, 43 3), having a household with a pet with diarrhoea (OR 2-39; CI 1P09, 5 25), and ingesting untreated water from lakes, rivers and streams (OR 4 16; CI 1.45, 11.9) were significant independent risk factors for becoming ill with campylobacter. Handling any whole chicken in the domestic kitchen that had been bought raw with giblets, or eating any dish cooked from chicken of this type in the home (OR 0 41-0-44; CI 0-24, 0 79) and occupational contact with livestock or their faeces (OR 0 44; CI 0-21, 0 92) were significantly associated with a decrease in the risk of becoming ill with campylobacter.

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