BBC reports that Salmonella Typhimurium DT193 illnesses are on the rise and no one is really sure whether they are linked or what the source might be.

Health officials are investigating how to stop a rise in cases of a salmonella strain which can leave patients severely ill, the BBC has learned. Cases of Salmonella Typhimurium DT193, rose 630% from 71 in 2004 to 518 in 2011 in England and Wales, said the Health Protection Agency. A Devon man diagnosed with DT193 poisoning in 2011 spent five days in hospital and is still suffering.

DT193 cases rose in the South West from 14 in 2004 to 73 in 2011. DT193, which is most common in beef and pork, is also found in unpasteurised milk, desserts and sandwiches according to the HPA.

It said in a statement: "The HPA study, which is ongoing, involves people who were ill being questioned about what they ate and activities they were involved in prior to becoming unwell.
"The aims of the study are to find any links between those who were unwell and give insights as to how to stop the increase in cases."

Devon builder Ian Mason, 54, was among eight people who contracted DT193 after attending a hog roast, identified by the HPA as a possible cause of the outbreak, in April 2011.

S. Typhimurium DT193 was linked to a bunch of European outbreaks in the 80s and 90s. Two of the big outbreaks were linked to pork products (in the UK and Italy).
 

Why bother editing; it’s all below in this letter from the current issue of Emerging Infectious Diseases, Identifying risk factors for shiga toxin–producing Escherichia coli by payment information.

During May and June 2011, a large outbreak of hemolytic uremic syndrome (HUS) and diarrhea caused by Shiga toxin–producing Escherichia coli (STEC) occurred, centered on northern Germany (1,2). Early on, salads and raw vegetables were suspected to be food vehicles (3). Also in May, the staff department of a local company informed the Health Protection Authority in Frankfurt in southwestern Germany about the rapidly increasing number of patients with bloody diarrhea and HUS among employees at 2 company office sites. Both sites were served by cafeterias run by the same caterer. Main dishes were prepared in the cafeterias’ kitchens and differed between the 2 sites. However, in both cafeterias various fresh foods from a salad bar and fruits, desserts, and daily asparagus dishes originated from the caterer’s main kitchen. The salad bar included 30 items. Suspecting that this outbreak was linked to the one in northern Germany, we conducted an outbreak investigation to confirm the epidemiologic link to focus epidemiologic and traceback investigations.

A face-to-face survey among hospitalized employees and by email among all other employees was conducted, which included personal details, symptoms, and information about general food eaten at the cafeterias. We defined outbreak cases as infections in employees of the company at 1 of the 2 sites who by May 23, 2011, were either hospitalized with bloody diarrhea or HUS or who self-reported onset of bloody diarrhea from May 8 through May 23. A total of 320 persons responded to the survey, and 285 (89%) of 320 of the responders stated they used the cafeterias; 60 employees fulfilled our case definition. Case-patients’ median age was 33 years (range 22–60 years); 36 (60%) of 60 were female. Thirty case-patients were hospitalized; HUS developed in 18 (30%) (Figure A1). Disease onsets occurred over 9 days. Beginning and magnitude of the outbreak were not different between cafeteria locations. Bacteriologic diagnostics for 11 patients yielded results that are compatible with the outbreak strain (4).

We used billing data from the cafeterias’ obligatory cashless payment system to ascertain risk factors for disease. A nested case–control study design was chosen, limited to a fraction of the cohort to obtain rapid risk estimates. Exposures included were purchases of any fruit, salad bar item, dessert, or asparagus dish in either cafeteria from May 2 through May 13. On the basis of customer identification numbers, the caterer provided billing information for persons with early cases (n = 23). Controls were randomly chosen persons from the caterer’s database whose disease status was checked against the survey information (n = 30) and who did not report symptoms of diarrhea (nonbloody), vomiting, or nausea during the same period. Univariable logistic regression was performed.
In univariable analysis, salad bar purchases were highly associated with illness (odds ratio 5.19; 95% CI 1.28–21.03), and desserts, fruit, and asparagus dishes were not (Table). Three (9%) of the case-patients remained unexposed to salad bar items according to the payment system data. The analysis of main courses purchased in 1 cafeteria revealed that no such meal had been consumed by >5 (22%) of 23 case-patients. Beginning May 23, the cafeterias were closed for 1 week, and salad sales were suspended for a longer period. There were no additional cases.

These results and the identification of the same rare serotype of O104:H4 renders this a satellite outbreak to the larger outbreak in northern Germany, which is the largest outbreak in terms of HUS ever described worldwide. Sprouts are believed to be the food vehicle (5). Sprouts available in the Frankfurt cafeteria salad bars were traced back to a producer of fenugreek sprouts, which appear to be the common source of primary cases in the entire outbreak (5). Sprout consumption could not be studied directly in Frankfurt because of the intense media attention on the sprout hypothesis once it had been announced. Also, it was thought that too much time had passed to successfully recall actually selected salad bar items consumed a few weeks previous.

Cafeteria billing information allowed for a rapid investigation while avoiding exposure misclassification attributable to ill-remembered food purchases (6). Using data sources independent of individual memory is quite useful. In previous studies, similar tools were successfully applied for the detection of outbreak vehicles. Credit card information was used during an investigation on STEC in beef sausages in Denmark (7), supermarket purchase records for STEC in Iceland (8), and grocery store loyalty card records for cyclosporiasis in Canada (9). Shopper card information was used in the United States in an outbreak of Salmonella enterica serovar Montevideo (10). However, billing information also could have introduced exposure misclassification, e.g., purchased food that was left uneaten or brought for colleagues. Analysis on ingredient level is often not possible. This study emphasizes the need for recall-independent investigation methods. In settings where such methods are available, they should be exploited early and relevant data saved from routine deletion.

Hendrik Wilking , Udo Götsch, Helma Meier, Detlef Thiele, Mona Askar, Manuel Dehnert, Christina Frank, Angelika Fruth, Gérard Krause, Rita Prager, Klaus Stark, Boris Böddinghaus, Oswald Bellinger, and René Gottschalk
Author affiliations: Robert Koch Institute, Berlin, Germany (H. Wilking, M. Askar, M. Dehnert, C. Frank, G. Krause, K. Stark); Health Protection Authority, Frankfurt am Main, Germany (U. Götsch, B. Böddinghaus, O. Bellinger, R. Gottschalk); Veterinary Service, Frankfurt am Main (H. Meier, D. Thiele); Robert Koch Institute, Wernigerode, Germany (A. Fruth, R. Prager)

Acknowledgment
We are grateful to the caterer, the employees, and the company management for their cooperation. We thank each member of the Robert Koch Institute HUS Investigation Team for their indispensable work and the coordinators of the German Postgraduate Training for Applied Epidemiology and the European Programme for Intervention Epidemiology Training for their help.

References
Frank C, Werber D, Cramer J, Askar M, Faber M, an der Heiden M, Epidemic profile of Shiga-toxin–producing Escherichia coli O104:H4 outbreak in Germany. N Engl J Med. 2011;365:1771–80. DOI PubMed
Wadl M, Rieck T, Nachtnebel M, Greutélaers B, An der Heiden M, Altmann D, Enhanced surveillance during a large outbreak of bloody diarrhoea and haemolytic uraemic syndrome caused by Shiga toxin/verotoxin–producing Escherichia coli in Germany, May to June 2011. Euro Surveill. 2011;16:pii:19893.
Frank C, Faber M, Askar M, Bernard H, Fruth A, Gilsdorf A, Large and ongoing outbreak of haemolytic uraemic syndrome, Germany, May 2011. Euro Surveill. 2011;16:pii:19878.
Bielaszewska M, Mellmann A, Zhang W, Köck R, Fruth A, Bauwens A, Characterisation of the Escherichia coli strain associated with an outbreak of haemolytic uraemic syndrome in Germany, 2011: a microbiological study. Lancet Infect Dis. 2011;11:671–6.PubMed
Buchholz U, Bernard H, Werber D, Böhmer MM, Remschmidt C, Wilking H, German outbreak of Escherichia coli O104:H4 associated with sprouts. N Engl J Med. 2011;365:1763–70. DOI PubMed
Decker MD, Booth AL, Dewey MJ, Fricker RS, Hutcheson RH, Schaffner W. Validity of food consumption histories in a foodborne outbreak investigation. Am J Epidemiol. 1986;124:859–63.PubMed
Ethelberg S, Smith B, Torpdahl M, Lisby M, Boel J, Jensen T, Outbreak of non-O157 Shiga toxin–producing Escherichia coli infection from consumption of beef sausage. Clin Infect Dis. 2009;48:e78–81. DOI PubMed
Sigmundsdottir G, Atladottir A, Hardardottir H, Gudmundsdottir E, Geirsdottir M, Briem H. STEC O157 outbreak in Iceland, September-October 2007. Euro Surveill. 2007;12(11):E071101.2.
Shah L, MacDougall L, Ellis A, Ong C, Shyng S, LeBlanc L. Challenges of investigating community outbreaks of cyclosporiasis, British Columbia, Canada. Emerg Infect Dis. 2009;15:1286–8. DOI PubMed
Centers for Disease Control and Prevention. Salmonella montevideo infections associated with salami products made with contaminated imported black and red pepper—United States, July 2009–April 2010. MMWR Morb Mortal Wkly Rep. 2010;59:1647–50.PubMed

Figure
Figure A1. Patients with Shiga toxin–producing Escherichia coli/hemolytic uremic syndrome (STEC/HUS) by onset of diarrhea and cafeteria visit (location A or B) during STEC/HUS outbreak at a company in Frankfurt, Germany,...
Table
Table. Univariable analysis of risk factors for bloody diarrhea among users of 2 cafeterias in Frankfurt, Germany, 2011
Suggested citation for this article: Wilking H, Götsch U, Meier H, Thiele D, Askar M, Dehnert M, et al. Identifying risk factors for Shiga toxin–producing Escherichia coli by payment information [letter]. Emerg Infect Dis [serial on the Internet] 2012 Jan [date cited]. http://dx.doi.org/10.3201/eid1801.111044
DOI: 10.3201/eid1801.111044

It’s not easy being a food safety investigator in the face of deep uncertainty.

So says Ron Doering, a past president of the Canadian Food Inspection Agency who practices food law in the Ottawa offices of Gowling Lafleur Henderson, in his latest Food Law column.

In the U.S., the largest foodborne outbreak in the last decade involved a rare strain of Salmonella Saintpaul thought to originate from tomatoes. The Food and Drug Administration (FDA) acted quickly, providing a public warning to avoid eating tomatoes until its investigation was complete. After several weeks and hundreds of tests and interviews, the FDA concluded that the problem was likely not tomatoes but rather hot peppers. Politicians rushed to microphones attacking the FDA for “destroying” the tomato industry. Of course, these are the same people who would have been outraged if tomatoes had been the source of the Salmonella and the FDA had not acted quickly.

While the FDA probably did the right things in the face of so much uncertainty, they should have communicated better. Tracing the source of foodborne illnesses is very complicated, especially for produce like tomatoes where there are no bar codes, no packages, and they are quickly consumed, often with other produce.

In the EU, the largest foodborne illness outbreak in the last decade, and one of the developed world’s most severe in modern times, took place this summer when a very rare strain of E. coli (O104:H4) got into the European food supply.

The first death was reported on May 24. The next day, the Robert Koch Institute announced that the early epidemiology indicated that the likely culprit was cucumbers, tomatoes or green salads. And later that day German officials announced that the rare strain had been found in the stools of five of the sick patients. The following day a German state-level agency announced triumphantly that it had found E. coli on Spanish cucumbers, though it had not yet tested for the strain.

On May 31, after testing for the strain, it was announced that the cucumbers were not to blame, by which time, of course, the Spanish cucumber industry was destroyed and German vegetable growers were suffering losses of $2.8 million per day as consumers quit eating all salads. Finally, on June 5 it was reported that “initial tests” (it was not tests, it was the result of epidemiological tracing) revealed that sprouts grown on an organic farm in Germany were “likely” the source of the problem, even though they couldn’t find a smoking sprout on the farm. Then on June 12 several victims of the O104 strain fell ill in France. They had no connection to the German organic farm. Attention turned to seeds, with the French blaming the British (I’m not making this up). Finally, on June 29 tracing determined the source of the problem as sprout seeds imported from Egypt in 2009. By this time there had been more than 50 deaths and well over 4,300 people seriously ill, including approximately 900 cases of patients with permanent kidney damage.

In both cases, with the benefit of hindsight, academics and the media roundly criticized the regulators as incompetent.

In a detailed review of the EU sprouts case, Peter Sandman, an expert on risk communication, concluded that the main failure of the regulators was in not being more forceful in proclaiming in their risk messaging the level of uncertainty in the case.

To me it seems there is a more basic problem, and it flows from the use of the language of risk, because “risk” disguises the deep uncertainty inherent in complex cases like these. These regulators were dealing with uncertainty, not risk — they were engaged in crisis management, not risk management.

People who forgot to mention they had eaten sprouts may have thrown disease trackers off the trail as they sought to trace the source of the deadly strain of E. coli that sickened more than 4,300 people and killed at least 50 in Europe this year, according to a study published in the New England Journal of Medicine.

While a definitive genetic link remains elusive, three separate lines of investigation point to sprouts as the means by which the deadly O1O4:H4 strain of the bacteria was spread, researchers led by Udo Buchholz at the Robert Koch Institute in Berlin, Germany’s disease-control agency.

Buchholz and colleagues wrote, “The one dish that frequently exposed guests to sprouts was the side salad, which contained tomatoes, cucumbers, three sorts of leaf salads, and sprouts. Sprouts may have been the ingredient that visitors recalled least in such a mixed salad.”

Buchholz and colleagues conducted three studies in parallel. The first involved asking patients hospitalized with E. coli infection about their recent food consumption, and comparing that with food eaten by uninfected people. It found that “the only significant variable was sprouts.”

The second study identified 10 groups of diners who ate at a restaurant in Luebeck between May 12 and 16. It found that among 115 people who had been served sprouts, 31 fell ill, compared with none of those who had not eaten sprouts.

The third investigation traced 41 clusters of infections to a producer in Lower Saxony, who grew sprouts from seeds that came from a “supplier X,” Buchholz and colleagues wrote, without identifying either the producer or the supplier. A European Commission task force said in July that the sprouts were probably grown from fenugreek seeds imported from Egypt in 2009. The researchers still don’t know whether the seeds were contaminated before, during or after export from Egypt.

In an accompanying editorial, Martin J. Blaser, M.D. from the Departments of Medicine and Microbiology, New York University, writes the chain of transmission appears to have begun in Egypt, with fecal contamination of fenugreek seeds by either humans or farm animals during storage or transportation, perhaps as long ago as 2009. The seeds then went to a European distributor and from there to farms in several countries. During sprout germination, bacteria multiplied and moved from farm to restaurants and consumers, as Buchholz et al. extensively detail in their study. The evidence for such a series of events is compelling, even though the organism was not identified at the earliest steps, since the trail often is cold in point-source outbreaks by the time investigators are able to conduct trace-back investigations.

German outbreak of Escherichia coli O104:H4 associated with sprouts
26.oct.11
The New England Journal of Medicine
Udo Buchholz, M.D., M.P.H., Helen Bernard, M.D., Dirk Werber, D.V.M., Merle M. Böhmer, Cornelius Remschmidt, M.D., Hendrik Wilking, D.V.M., Yvonne Deleré, M.D., Matthias an der Heiden, Ph.D., Cornelia Adlhoch, D.V.M., Johannes Dreesman, Ph.D., Joachim Ehlers, D.V.M., Steen Ethelberg, Ph.D., Mirko Faber, M.D., Christina Frank, Ph.D., Gerd Fricke, Ph.D., Matthias Greiner, D.V.M., Ph.D., Michael Höhle, Ph.D., Sofie Ivarsson, M.Sc., Uwe Jark, D.V.M., Markus Kirchner, M.D., M.P.H., Judith Koch, M.D., Gérard Krause, M.D., Ph.D., Petra Luber, Ph.D., Bettina Rosner, Ph.D., M.P.H., Klaus Stark, M.D., Ph.D., and Michael Kühne, D.V.M., Ph.D.
http://www.nejm.org/doi/full/10.1056/NEJMoa1106482?query=featured_home
Human infection with Shiga-toxin–producing Escherichia coli is a major cause of postdiarrheal hemolytic–uremic syndrome. This life-threatening disorder, which is characterized by acute renal failure, hemolytic anemia, and thrombocytopenia, typically affects children under the age of 5 years. Shiga-toxin–producing E. coli O157 is the serogroup that is most frequently isolated from patients with the hemolytic–uremic syndrome worldwide.1
In May 2011, a large outbreak of the hemolytic–uremic syndrome associated with the rare E. coliserotype O104:H4 occurred in Germany.2-5 The main epidemiologic features were that the peak of the epidemic was reached on May 21 and May 224,5 and that the vast majority of case subjects either resided or had traveled in northern Germany. Almost all patients from other European countries or from North America had recently returned from northern Germany.2,6,7 Of the affected case subjects, 90% were adults, and more than two thirds of case subjects with the hemolytic–uremic syndrome were female.4
Early studies in Hamburg suggested that infections were probably community-acquired and were not related to food consumption in a particular restaurant. A first case–control study that was conducted on May 23 and 24 suggested that raw food items, such as tomatoes, cucumbers, or leaf salad,3 were the source of infection. The consumption of sprouts, which was previously implicated in outbreaks of Shiga-toxin–producing E. coli in the United States8 and Japan,9 was mentioned by only 25% of case subjects in exploratory interviews, so consumption of sprouts was not tested analytically.
This report describes the investigations that were conducted by the federal agencies under the auspices of the German Ministry of Health and the Ministry of Food, Agriculture, and Consumer Protection, as well as by the respective state agencies, to identify the vehicle of infection of this international outbreak.