M onkeypox is a reemerging zoonosis caused by Monkeypox virus (MPXV), a member of the genus Orthopoxvirus. MPXV is related to Variola virus, the causative agent of smallpox. Although infections with these 2 viruses share many clinical features, monkeypox is generally less severe than smallpox (1). Among unvaccinated persons, the monkeypox case-fatality rate can be up to 10%, although casefatality rates are lower for infection with the West African than the Central African clade of MPXV (2). In recent years, the number of cases and geographic spread of monkeypox have been increasing, possibly because of waning immunity to smallpox (3-5). Before 2018, the only human cases of monkeypox outside Africa occurred in the United States in 2003; that outbreak was associated with rodents imported from Ghana, and human-to-human transmission did not occur (6). In September 2018, Public Health England (PHE) was notified of 2 unrelated cases of monkeypox affecting travelers who had recently returned from Nigeria (7). We describe transmission of monkeypox virus from the second of these cases to a healthcare worker (HCW) and the public health measures implemented to prevent further cases. The Cases On September 6, 2018, a man with a maculopapular rash, fever, lymphadenopathy, and a 1-week history of feeling generally unwell (patient 2) sought care at a hospital in England (7). He was admitted to a singleoccupancy room in the acute medical unit. The staff attending the patient wore standard personal protective equipment (PPE), consisting of disposable aprons and gloves. Because a travel-associated infection was considered possible, patient 2 was transferred to an isolation room on September 7, 2018. Three days later, a clinical diagnosis of suspected monkeypox was made, and infection prevention and control precautions for a high-consequence infectious disease (HCID) were implemented (e.g., enhanced PPE consisting of disposable gown, disposable gloves, filtering facepiece 3 respirator, and face shield or goggles). The patient was transferred to an Airborne HCID Treatment Centre, and monkeypox was confirmed by laboratory testing at PHE (7). Although the risk to the public was considered to be very low, a precautionary approach was adopted. Possible hospital and community contacts of patient 2 were identified and assessed for risk (Table).

In early September 2018, two cases of monkeypox were reported in the United Kingdom (UK), diagnosed on 7 September in Cornwall (South West England) and 11 September in Blackpool (North West England). The cases were epidemiologically unconnected and had recently travelled to the UK from Nigeria, where monkeypox is currently circulating. We describe the epidemiology and the public health response for the first diagnosed cases outside the African continent since 2003.

Discussions from the expert group supported joint working across countries to better monitor the epidemiology and possible changes in risk of virus acquisition at a European level. There was agreement to share surveillance strategies and algorithms but also importantly the collation of HEV data from human and animal populations. These data collected at a European level would serve the 'One Health' approach to better informing on human exposure to HEV.

The outbreak was probably foodborne.

Hepatitis E virus (HEV) is an under-recognised cause of acute hepatitis in high-income countries. The purpose of this study was to provide an overview of testing, diagnosis, surveillance activities, and data on confirmed cases in the European Union/European Economic Area (EU/EEA). A semi-structured survey was developed and sent to 31 EU/EEA countries in February 2016, 30 responded. Twenty of these countries reported that they have specific surveillance systems for HEV infection. Applied specific case definition for HEV infection varied widely across countries. The number of reported cases has increased from 514 cases per year in 2005 to 5,617 in 2015, with most infections being locally acquired. This increase could not be explained by additional countries implementing surveillance for HEV infections over time. Hospitalisations increased from less than 100 in 2005 to more than 1,100 in 2015 and 28 fatal cases were reported over the study period. EU/EEA countries are at different stages in their surveillance, testing schemes and policy response to the emergence of HEV infection in humans. The available data demonstrated a Europe-wide increase in cases. Standardised case definitions and testing policies would allow a better understanding of the epidemiology of HEV as an emerging cause of liver-related morbidity.

HEV infection rates are dynamic in England and Wales, influenced by changing trends in indigenously-acquired cases. The recent increase in indigenous cases and the emergence of indigenous viruses not commonly circulating prior to 2010 suggest that the risk of acquiring HEV has changed.

Indigenously acquired hepatitis E infections have increased substantially in England and Wales since 2010. Epidemiological investigations were undertaken to determine risk factors for the acquisition of infection. A case-control study (25 cases, 75 controls) was used to test the hypothesis that hepatitis E infection was related to consumption of pork products. In a multivariable model, consumption of pork pie [odds ratio (OR) 6·33, 95% confidence interval (CI) 1·41-28·48, P = 0·009] and consumption of ham and sausages purchased from a major UK supermarket chain (OR 10·12, 95% CI 1·68-60·81, P = 0·023) were significantly associated with indigenous infection. The consumption of sausages and ham purchased from the supermarket was highly correlated; however. separate models showed that each variable was significantly associated with infection (OR 7·59, 95% CI 1·81-31·84, P = 0·004 and OR 10·98, 95% CI 1·84-65·35, P = 0·003, respectively). Although contamination of sausages with HEV has previously been shown this study also raises concerns about other processed pork products and whether current practice in preparing these products is sufficient to prevent transmission of HEV.

I d e n t if i ca t i o n of en t e ro p a t h oge n i c Escherichia co/iSummary. Strains of Escherichia coli from sporadic cases of diarrhoea and belonging to serotypes 044 : H 18,055 : H7,O 1 1 lab : H2 1,011 1 ab : H25 or 0 126 : H27 were examined for virulence properties. With the exception of 0 1 1 lab: H25 these are considered to be classical enteropathogenic E. coli (EPEC) serotypes. The strains had been isolated in Britain from the faeces of children < 3 years old. Of the serotypes examined, 7 of 13 044 : H 18 strains, all of 10 0 1 1 lab : H21 strains and 13 of 21 0126 : H27 strains belonged to the enteroaggregative class of E. coli (EAggEC) that attached to HEp-2 cells in the characteristic aggregative pattern and hybridised with the EAggEC probe. They also caused mannose-resistant haemagglutination of rat erythrocytes, a property which may be a useful marker for their identification. Strains of 044 : H18 with similar properties were also isolated from three small outbreaks in Britain, one of which involved elderly patients. EAggEC have not been considered previously as aetiological agents of diarrhoea in developed countries and have rarely been reported as belonging to EPEC serotypes. All 15 055 : H7 strains and seven of eight 0 1 1 lab: H25 strains were also considered to be potentially diarrhoeagenic as they gave localised attachment (LA) to HEp-2 cells that resulted in a positive fluorescence actinstaining test. This test is considered to correlate with the attaching-and-effacing virulence mechanisms of EPEC in vivo. None of the strains in this study hybridised with the EPEC adherence-factor (EAF) probe. Neither the aggregative EPEC nor the LA-positive EAFnegative EPEC described here would be identified in epidemiological surveys when the EAF probe is used in the absence of cell tests.