E. coli O26, HUS and dairy

In their recent article in Eurosurveillance, Germinario et al. describe a community-wide outbreak of Shiga toxin 2-producing Escherichia coli (STEC) O26:H11 infections associated with haemolytic uraemic syndrome (HUS) and involving 20 children between 11 and 78 months of age in southern Italy during the summer 2013 [1]. The investigation identified an association between STEC infection and consumption of dairy products from two local milk-processing establishments. We underline striking similarities to a recent multi-country STEC O26 outbreak in Romania and Italy and discuss the challenges that STEC infections and their surveillance pose at the European level.

e-coli-colbertIn March 2016, Peron et al. published, also in Eurosurveillance, early findings of the investigation of a community-wide STEC infection outbreak in southern Romania [2]. As at 29 February 2016, 15 HUS cases with onset of symptoms after 24 January 2016, all but one in children less than two years of age, had been identified, three of whom had died. Aetiological confirmation was retrospectively performed through serological diagnosis and six cases were confirmed with STEC O26 infection. Shortly after this publication, and following the identification of the first epidemiologically-linked case in central Italy, the European Centre for Disease Prevention and Control (ECDC) and the European Food Safety Authority (EFSA) published a joint Rapid Outbreak Assessment [3]. The Italian and Romanian epidemiological, microbiological and environmental investigations implicated products from a milk-processing establishment in southern Romania as a possible source of infection. The dairy plant exported milk products to at least four European Union (EU) countries. The plant was closed in March 2016 and the implicated food products recalled or withdrawn from the retail market.

Pulsed Field Gel Electrophoresis (PFGE) and whole genome sequencing (WGS) analyses did not establish a microbiological link between the Italian (2013) and the Romanian/Italian (2016) outbreaks (personal communication, Stefano Morabito, October 2016). However, the epidemiological similarities between the two community-wide outbreaks associated with HUS and STEC O26 infections, mostly affecting young children and implicating dairy products, are notable. While raw milk and unpasteurised dairy products are well known potential sources of STEC infection, milk products, as highlighted by Germinaro et al. [1], have been rarely implicated in community-wide STEC outbreaks in the past, emphasising an emerging risk of STEC O26 infection associated with milk products.

Reporting of STEC O26 infections has been steadily increasing in the EU since 2007, partly due to improved diagnostics of non-O157 sero-pathotypes [4]. The attention to non-O157 STEC sero-pathotypes rose considerably after the severe STEC O104 outbreak that took place in Germany and France in 2011 during which almost 4,000 cases and more than 50 deaths were reported [5]. In light of the recently published outbreaks related to dairy products and the simultaneous increased reporting of isolations of STEC O26 from milk and milk products in the EU/European Economic Area (EEA) [6], strengthening STEC surveillance in humans and food and enhancing HUS surveillance in children less than five years of age is warranted. Paediatric nephrologists should be sensitised to this effect

Community-wide outbreaks of haemolytic uraemic syndrome associated with Shiga-toxin producing Escherichia coli O26 in Italy and Romania: A new challenge for the European Union

Eurosurveillance, Volume 21, Issue 49, 08 December 2016, DOI: http://dx.doi.org/10.2807/1560-7917.ES.2016.21.49.30420

E Severi, F Vial, E Peron, O Mardh, T Niskanen, J Takkinen


Foodborne Clostridium botulinum intoxication from mass produced foodstuffs in Europe

It’s botulism week at Eurosurveillance as the on-line journal summarizes three different and recent Europe-based botulism outbreaks, which represents an alarming increase over previous years.

In an overview editorial, Cowden notes the incidence of botulism in the European Union (EU) is described elsewhere, but that from 2006 and 2008, 477 confirmed cases were notified: an average of 119 cases per year, with a range of 104 to 132, and no discernable trend.

The surveillance of cases of botulism in the EU includes the three main forms of the disease but does not distinguish between them.

Food-borne botulism is caused by the ingestion of toxin produced by organisms in an anaerobic environment. It usually results from inadequately sterilised domestically canned or bottled foods.

Intestinal botulism is caused by the production in the gut of toxin by organisms which have been ingested and have proliferated. This form predominantly affects infants under a year old, often associated with the consumption of honey.

Wound botulism is caused by the production of toxin by organisms introduced into wounds. This is often associated with dirty wounds, including those following injecting drug use.

Since 2009, Eurosurveillance has published only four reports of outbreaks of food-borne botulism in Europe and only three resulted from consumption of widely distributed, commercially produced foods.

Despite only one of the four outbreaks being due to domestically prepared food, home-preserved food is generally acknowledged to be the major cause of botulism in those EU countries that have had most cases in recent years and outbreaks resulting from mass produced foods are rare.

Against this background, from September to November 2011, there were three outbreaks in three different countries in Europe. In the outbreaks which feature in this issue of Eurosurveillance, the vehicles of intoxication were demonstrated, on the basis of strong toxicological and descriptive epidemiological evidence, to have been widely distributed, commercially produced foods.

These three outbreaks present intriguing differences and similarities.

In two outbreaks, the Finnish and the Scottish, cases were confined to single households. In France cases occurred in two household clusters.

In the French and Finnish outbreaks the vehicles included olives: olive tapenades in the French outbreak, and almond-stuffed olives in the Finnish. In the Scottish outbreak, the vehicle was korma sauce.

In all three outbreaks the vehicle of intoxication was marketed in glass jars with screw-top lids.

In the French and the Scottish outbreaks the food was produced and distributed within the country of origin. In the Finnish outbreak, the food was distributed internationally from another country, Italy.

In the Finnish and the Scottish outbreaks the food was produced in industrialized units. In the French outbreak the producer was described as an “artisanal producer” although the tapenade was commercially produced and widely distributed.

In the French and the Scottish outbreaks the toxin was type A. In the Finnish outbreak it was type B.

In two outbreaks, the Finnish and the French, defects potentially explaining the contamination were identified. In the Finnish outbreak, seals in other jars from the same batch were found to have defects, although none was found to be contaminated. In the French outbreak an improper sterilization process was identified. In the Scottish outbreak the food originated from a state-of-the-art food-production facility where intensive investigation has yet to find any shortcomings, and no post-production event has been identified which could explain the contamination.

The number of cases in all three outbreaks was surprisingly low if a production fault is assumed to have affected the production of at least a whole batch of jars.

This is particularly true of the Scottish outbreak where only one household was affected, and which could be explained by the contamination of a single jar from a batch of 1,836 jars. Likewise, the Finnish outbreak affected a single household, and could be explained by only one contaminated jar of stuffed olives, despite the batch being part of a lot of 900 imported into Finland, and the product having been exported to many countries in Europe and beyond.

Only in the French outbreak does the contamination of more than one jar need to be hypothesized to explain the cases – and even here, contamination of only two jars could explain the cases. The size of the batch in the French outbreak was approximately 60 pots.

The other 3 outbreak write-ups are available at the urls below, and full-text, as always, on bites-l.




The role of asymptomatic food preparers: 3 norovirus outbreaks in Europe

Norovirus outbreaks are becoming better recognized and are popping up in diverse scenarios.

Today’s issue of Eurosurveillance presents three different norovirus outbreaks, each with its own investigative twists and turns. Excerpts from the three reports are below.

Mayet et al., report that on April 13/11, the medical service of a French military parachuting unit reported an outbreak of acute gastroenteritis involving 147 persons among the military personnel. Meals suspected to have caused the outbreak (pasta and some raw vegetables) were tested for norovirus by PCR. The same norovirus (genogroup I) was found in some of the food items consumed by the cases and in a cook who prepared the meals.

At French military base canteens, meal items are routinely sampled and samples are kept for five days. We tested for norovirus the water of the drinking fountains and the food items served and sampled in the canteen on 11 and 12 April, which were suspected to be associated with the outbreak following the analytical study. The extracted RNA was tested for norovirus by real-time RT-PCR [3]. Pasta was tested by culture for Bacillus cereus which was initially suspected to have caused the outbreak by the physicians who treated the cases. In addition, water from the drinking fountain was tested by culture for coliform germs. For logistical reasons, no samples were requested from the cases, apart from a cook who had prepared the meals and who had fallen ill before the outbreak. The stool sample from the cook was tested for norovirus by PCR as described.

This norovirus-related food-borne disease outbreak involving 147 cases occurred during a parachuting exercise on the night of 12 April and affected significantly the activities of the military unit. It is interesting to note that another outbreak of acute gastroenteritis occurred between 10 and 12 April among residents of a retirement home in the same geographical area, in which the same cook involved in the outbreak in the military unit prepared food on 9 and 10 April. However, the outbreak in the nursing home was only suspected after interrogation of the ill cook; it had not been reported to the health authorities and consequently, it had not been investigated, but it is likely that it was also caused by norovirus considering that around 50% of acute gastroenteritis outbreaks in industrialised countries are related to this agent. Other norovirus outbreaks related to raw vegetables have been described in the past in other military units. The episode described here illustrates once more that food-borne disease outbreaks can easily occur in such settings and stricter hygiene measures may need to be considered.

Guzman-Herrador et al., report that 56 people were affected with gastroenteritis after attending a one-day meeting in a high-quality hotel in the centre of Oslo, Norway, at the end of January 2011. A complete outbreak investigation was carried out. The microbiological investigation confirmed that the outbreak was caused by norovirus. All participants at the meeting were invited by email to complete an online questionnaire asking for information on demographic data, symptoms and food consumption. The results of the epidemiological investigation of the food items served were inconclusive and the source and transmission route of this outbreak remains unclear. However, the environmental investigation highlighted several irregularities in the kitchen that may have enabled the spread of the virus. Specific cleaning procedures and rules were set up for the kitchen staff. As a consequence of this outbreak investigation, the hotel is planning to change its internal routine protocols, for example, samples of food items served at every meal during an event will be stored.

The irregularities that the Food Safety Authority’s inspection found in the kitchen may have enabled the spread of the virus. Handling of ready-to-eat foods by infected food handlers is commonly identified as a contributing factor in outbreaks caused by norovirus. However, the role of kitchen employees or food handlers in the outbreak reported here remains unclear since none of those in the hotel reported any symptoms to the Food Safety Authority and no information was available regarding the health status of the food handlers who produced some of the food items outside the hotel. The importance of identifying asymptomatic food handlers shedding the virus is also well described in the literature: such people can also be a contributing factor in norovirus outbreaks. We do not know if asymptomatic food handlers were involved in the spread of the virus in this outbreak as the employees were not asked to provide stool samples.

Finally, Nicolay et al., report that in March 2009, the Department of Public Health in Dublin, Ireland, was notified of a cluster of four gastroenteritis cases among people who attended a family lunch in a Dublin hotel. A retrospective cohort study was carried out. An outbreak case was defined as an attendee who developed diarrhoea and/or vomiting in the 60 hours following the lunch. Of 57 respondents, 27 met the case definition. Consumption of egg mayonnaise, turkey with stuffing or chicken sandwiches were each associated with increased risk of gastroenteritis. An environmental investigation established that before notification of the cluster, there had been unreported gastroenteritis among staff at the hotel. The earliest symptomatic person identified was a staff member who had vomited in the staff toilets but had not reported it. The sandwiches had most likely been contaminated by three asymptomatic kitchen food handlers who had used the same toilets. Stool samples were submitted by eight cases and 10 staff members. All eight cases and three asymptomatic food handlers on duty at the lunch tested positive for norovirus genogroup II.4 2006. Our analysis suggests that asymptomatic food-handlers can be responsible for norovirus transmission.