All the news just repeats itself: Leafy greens in public

In October, 1996, a 16-month-old Denver girl drank Smoothie juice manufactured by Odwalla Inc. of Half Moon Bay, California. She died several weeks later; 64 others became ill in several western U.S. states and British Columbia after drinking the same juices, which contained unpasteurized apple cider — and E. coli O157:H7. Investigators believed that some of the apples used to make the cider might have been insufficiently washed after falling to the ground and coming into contact with deer feces (Powell and Leiss, 1997) not that washing would do much.

Almost 10 years later, on Sept. 14, 2006, the U.S. Food and Drug Administration announced that an outbreak of E. coli O157: H7 had killed a 77-year-old woman and sickened 49 others (United States Food and Drug Administration, 2006). The outbreak ultimately killed four and sickened at least 200 across the U.S. This was documented-outbreak 29 linked to leafy greens, but also apparently the tipping point for growers to finally get religion about commodity-wide food safety, following the way of their farmer friends in California, 10 years later.

In the decade between these two watershed outbreaks, almost 500 outbreaks of foodborne illness involving fresh produce were documented, publicized and led to some changes within the industry, yet what author Malcolm Gladwell would call a tipping point — “a point at which a slow gradual change becomes irreversible and then proceeds with gathering pace” — in public awareness about produce-associated risks) did not happen until the spinach E. coli O157:H7 outbreak in the fall of 2006. At what point did sufficient evidence exist to compel the fresh produce industry to embrace the kind of change the sector has heralded since 2007? And at what point will future evidence be deemed sufficient to initiate change within an industry?

The 1993 outbreak of E. coli O157:H7 associated with undercooked hamburgers at the Jack-in-the-Box fast food chain propelled microbial food safety to the forefront of public awareness, at least in the U.S. (Powell and Leiss, 1997). In 1996, following extensive public and political discussions about microbial food safety in meat, the focus shifted to fresh fruits and vegetables, following an outbreak of Cyclospora cayetanesis ultimately linked to Guatemalan raspberries that sickened 1,465 in 21 U.S. states and two Canadian provinces (U.S. Centers for Disease Control and Prevention, 1997). That same year, Beuchat (1996) published a review on pathogenic microorganisms in fresh fruits and vegetables and identified numerous pathways of contamination.

By 1997, researchers at CDC were stating that pathogens could contaminate at any point along the fresh produce food chain — at the farm, processing plant, transportation vehicle, retail store or foodservice operation and the home — and that by understanding where potential problems existed, it was possible to develop strategies to reduce risks of contamination (Tauxe et al., 1997). Researchers also reported that the use of pathogen-free water for washing would minimize risk of contamination (Suslow, 1997; Beuchat, 1998).

Beuchat and Ryu (1997) reported in a review that sources of pathogenic microorganisms for produce included:

Preharvest

  • Feces
  • Soil
  • Irrigation water
  • Water used to apply fungicides, insecticides
  • Green or inadequately composted manure
  • Air (dust)
  • Wild and domestic animals (including fowl and reptiles)
  • Insects
  • Human handling

Postharvest

  • Feces
  • Human handling (workers, consumers)
  • Harvesting equipment
  • Transport containers (field to packing shed)
  • Wild and domestic animals (including fowl and reptiles)
  • Insects
  • Air (dust)
  • Wash and rinse water
  • Sorting, packing, cutting, and further processing equipment
  • Ice
  • Transport vehicles
  • Improper storage (temperature, physical environment)
  • Improper packaging (including new packaging technologies)
  • Cross-contamination (other foods in storage, preparation, and display areas)
  • Improper display temperature.

kFresh fruits and vegetables were identified as the source of several outbreaks of foodborne illness in the early 1990s, especially leafy greens (Table 1).

Date Product Pathogen Cases Setting/dish State
Apr-92 Lettuce S. enteriditis 12 Salad VT
Jan-93 Lettuce S. Heidelberg 18 Restaurant MN
Jul-93 Lettuce Norovirus 285 Restaurant IL
Aug-93 Salad E. coli O157:H7 53 Salad Bar WA
Jul-93 Salad E. coli O157:H7 10 Unknown WA
Sep-94 Salad E. coli O157:H7 26 School TX
Jul-95 Lettuce E. coli O153:H48 74 Lettuce MT
Sep-95 Lettuce E. coli O153:H47 30 Scout Camp ME
Sep-95 Salad E. coli O157:H7 20 Ceasar Salad ID
Oct-95 Lettuce E. coli O153:H46 11 Salad OH
May-96 Lettuce E. coli O157:H10 61 Mesclun Mix ML
Jun-96 Lettuce E. coli O153:H49 7 Mesclun Mix NY

Outbreaks of foodborne illness related to leafy greens, 1992-1996.

Dave Gombas told an International Association for Food Protection symposium on leafy green safety on Oct. 6, 2006 in Washington, D.C. that if growers did everything they were supposed to do — in the form of good agricultural practices — and it was verified, there may be fewer outbreaks. He then said government needs to spend a lot more on research.

Wow. The same person who has vacillated between the Produce Marketing Association and the U.S. Food and Drug Administration for the past couple of decades (all you critics who complain about folks jumping back-and-forth-and-back as part of a genetically-engineered conspiracy may want to look at the all-natural, all-good-for-ya produce sector) pronounced on grower verification in which nothing has been done.

Since we were on the same panel in Washington, in 2006, I asked Gombas, why is the industry calling for more investment in research about the alleged unknowns of microbial contamination of produce when the real issue seems to be on-farm delivery and verification? Hiding behind the unknown is easy, working on verifying what is being done is much harder.

More calls for research.

Nothing on human behavior in a fresh produce environment.

It’s just another case of saying the right things in public, but failing to acknowledge what happens on individual farms. Verification is tough. Auditing may not work, because many of these outbreaks happened on third -party audited operations. Putting growers in a classroom doesn’t work, and there’s no evidence that begging for government oversight yields a product that results in fewer sick people.

In 1999, several more outbreaks of Shiga-toxin producing E. coli (STEC) were linked to leafy greens (Table 2), and the U.S. group, the United Fresh Fruit and Vegetable Association, developed and published HACCP-based food safety guidelines for industry (United Fresh Fruit and Vegetable Association, 1999).

Date Product Pathogen Cases Setting/dish State
Feb-99 Lettuce E. coli O157:H9 65 Restaurant NE
Jun-99 Salad E. coli O111:H8 58 Texas Camp TX
Sep-99 Lettuce E. coli O157:H11 6 Iceberg WA
Oct-99 Lettuce E. coli O157:H7 40 Nursing Home PA
Oct-99 Lettuce E. coli O157:H7 47 Restaurant OH
Oct-99 Salad E. coli O157:H7 5 Restaurant OR

Table 2. 1999 U.S. outbreaks of STEC linked to leafy greens

By 2000, Rafferty and colleagues demonstrated that E. coli could spread on-farm in plant production cuttings from one contaminated source, magnifying an outbreak to a whole farm (Rafferty et al., 2000). A 2001 outbreak of Shigella flexneri (886 ill) in tomatoes further focused public and scientific attention onto fresh produce.

Solomon and colleagues (2002a) discovered that the transmission of E. coli O157:H7 to lettuce was possible through both spray and drip irrigation. They also found that the pathogen persisted on the plants for 20 days following application and submerging the lettuce in a solution of 200ppm chlorine did not eliminate all viable E.coli O157:H7 cells, suggesting that irrigation water of unknown microbial quality should be avoided in lettuce production (Solomon et al., 2002a). In a follow-up experiment, Solomon and colleagues (2002b) explored the transmission of E. coli O157:H7 from manure-contaminated soil and irrigation water to lettuce plants. The researchers recovered viable cells from the inner tissues of the lettuce plants and found that the cells migrated to internal locations in plant tissue and were thus protected from the action of sanitizing agents. These experiments demonstrated that E. coli O157:H7 could enter the lettuce plant through the root system and migrate throughout the edible portion of the plant (Solomon et al., 2002b). Such results were widely reported in general media.

During this time, several outbreaks of E. coli were again linked to lettuce and salad (Table 3).

Date Product Pathogen Cases Setting/dish State
Oct-00 Salad E. coli O157:H7 6 Deli IN
Nov-01 Lettuce E. coli O157:H7 20 Restaurant TX
Jul-02 Lettuce E. coli O157:H8 55 Bagged, Tossed WA
Nov-02 Lettuce E. coli O157:H7 13 Restaurant IL
Dec-02 Lettuce E. coli O157:H7 3 Restaurant MN

Table 3: Leafy green outbreaks of STEC, 2000 — 2002.

 In 2003, according to Mexican growers, the market impact of an outbreak of hepatitis A traced to exported green onions lasted up to 4 months while prices fell 72 per cent (Calvin et al., 2004). Roma tomatoes were identified as the source of a salmonellosis outbreak that resulted in over 560 cases in both Canada and the US (CDC 2005).

During 2003-2005, several additional outbreaks of E. coli O157:H7 were linked to fresh leafy greens, including one multi-state outbreak involving Dole bagged lettuce (Table 4). 

Date Product Pathogen Cases Setting/dish State
Sep-03 Lettuce E. coli O157:H7 51 Restaurant CA
Nov-03 Spinach E. coli O157:H7 16 Nursing Home CA
Nov-04 Lettuce E. coli O157:H7 6 Restaurant NJ
Sep-05 Lettuce E. coli O157:H7 11 Dole, bagged Multiple

Table 4: Leafy green STEC outbreaks, 2003 — 2005.

During 2005–2006, four large multistate outbreaks of Salmonella infections associated with eating raw tomatoes at restaurants occurred in the U.S., resulting in 459 culture-confirmed cases of salmonellosis in 21 states. Investigations determined that the tomatoes had been supplied to restaurants either whole or precut from tomato fields in Florida, Ohio, and Virginia (CDC, 2006).

Allwood and colleagues (2004) examined 40 items of fresh produce taken from a retail setting in the U.S. that had been preprocessed (including cut, shredded, chopped or peeled) at or before the point of purchase. They found fecal contamination indicators (E. coli, F-specific coliphages, and noroviruses) were present in 48 per cent of samples.

 Researchers in Minnesota conducted a small-scale comparative study of organic versus conventionally grown produce. They found that while all samples were virtually free of pathogens, E. coli was 19 times more prevalent on produce acquired from the organic farms (Mukherjee et al., 2004). They estimated that this was due to the common use of manure aged for less than a year. Use of cattle manure was found to be of higher risk as E. coli was found 2.4 times more often on farms using it than other animal manures (Mukherjee et al., 2004).

On Sept. 14, 2006, the U.S. Food and Drug Administration (2006) issued a public statement warning against the consumption of bagged fresh spinach.

“Given the severity of this illness and the seriousness of the outbreak,” stated Dr. Robert Brackett, Director of FDA’s Center for Food Safety and Applied Nutrition (CFSAN), “FDA believes that a warning to consumers is needed (United States Food and Drug Administration, 2006).”

That is no different from the sometimes conflicting messages coming from FDA today about the E. coli O157:H7 outbreak on lettuce that originated in Yuma, Arizona: these public health folks are figuring it out on the go.

Sean Rossman of USA Today reports today that in the current E. coli O157:H7 outbreak linked to Yuma lettuce, 70% of those who’ve gotten sick are female.

Similarly, when leafy greens were the culprit of an E. coli outbreak last year, 67% of those infected were women or girls. In 2016, females were 73% of those ill from an outbreak in alfalfa sprouts, notes the U.S. Centers for Disease Control and Prevention.

Here are some suggestions:

  • The first line of defense is the farm, not the consumer.
  • All ruminants — cows, sheep, goats, deer — can carry dangerous E. coli like the O157:H7 strain that sickened people in the spinach outbreak, as well as the Taco Bell and Taco Johns outbreaks ultimately traced to lettuce.
  • Any commodity is only as good as its worst grower.

We’ve had a few peer-reviewed thoughts on these topics:

Powell, D.A. and Chapman, B. 2007. Fresh threat: what’s lurking in your salad bowl?. Journal of the Science of Food and Agriculture. 87: 1799-1801.

Implementing On-Farm Food Safety Programs in Fruit and Vegetable Cultivation, Improving the Safety of Fresh Fruit and Vegetables

Luedtke, A., Chapman, B. and Powell, D.A. 2003. Implementation and analysis of an on-farm food safety program for the production of greenhouse vegetables. Journal of Food Protection. 66:485-489.

Powell, D.A., Bobadilla-Ruiz, M., Whitfield, A. Griffiths, M.G.. and Luedtke, A. 2002. Development, implementation and analysis of an on-farm food safety program for the production of greenhouse vegetables in Ontario, Canada. Journal of Food Protection. 65: 918- 923.

Surveys suck, publication before peer-review sucks, and why aren’t Canadian journalists more discerning?

There’s not many real journalists left, so PR flaks rule the ether.

It’s not surprising that repeat offender of PR-before-peer-review Sylvan Charlebois has climbed the org chart, moving from the University of Guelph to dean thingy at Dalhousie University’s Faculty of Management in Halifax, Nova Scotia (guess that’s like going from Guelph to be president of the University of Windsor).

The best and brightest get promoted up the chain.

The public relations machinery at Dalhousie University announced breathlessly on April 5, 2018 that Canadians are confused about food recalls.

And the National Post faithfully reprinted the PR.

“A new study from Dalhousie University’s Faculty of Management shows that many Canadians aren’t getting enough information about food recalls. In a recent survey, most respondents underestimated the number of food recalls that happened in 2017, and many had trouble correctly recollecting recalls that have occurred.”

The new study is just that – a study.

It has not been peer-reviewed, it has not been published, the kind of standards scientists are used too.

So, no discussion from me – other than PR-before-publication is a dangerous trap.

The best thing Halifax has going for it is underrated power-pop band, Sloan, who released new music a couple of weeks ago.

Raw is risky: Salmonella growth on sprouts and microgreens

Microgreens, like sprouts, are relatively fast-growing products and are generally consumed raw. Moreover, as observed for sprouts, microbial contamination from preharvest sources may also be present in the production of microgreens.

In this study, two Salmonella enterica serovars (Hartford and Cubana), applied at multiple inoculation levels, were evaluated for survival and growth on alfalfa sprouts and Swiss chard microgreens by using the most-probable-number (MPN) method. Various abiotic factors were also examined for their effects on Salmonella survival and growth on sprouts and microgreens. Community-level physiological profiles (CLPPs) of sprout/microgreen rhizospheres with different levels of S. enterica inoculation at different growth stages were characterized by use of Biolog EcoPlates. In the seed contamination group, the ability of S. enterica to grow on sprouting alfalfa seeds was affected by both seed storage time and inoculation level but not by serovar. However, the growth of S. enterica on Swiss chard microgreens was affected by serovar and inoculation level. Seed storage time had little effect on the average level of Salmonella populations in microgreens. In the irrigation water contamination group, the growth of Salmonella on both alfalfa sprouts and microgreens was largely affected by inoculation level. Surprisingly, the growth medium was found to play an important role in Salmonella survival and growth on microgreens. CLPP analysis showed significant changes in the microbial community metabolic diversity during sprouting for alfalfa sprouts, but few temporal changes were seen with microgreens. The data suggest that the change in rhizosphere bacterial functional diversity was dependent on the host but independent of Salmonella contamination.

Sprouts and microgreens are considered “functional foods,” i.e., foods containing health-promoting or disease-preventing properties in addition to normal nutritional values. However, the microbial risk associated with microgreens has not been well studied. This study evaluated Salmonella survival and growth on microgreens compared to those on sprouts, as well as other abiotic factors that could affect Salmonella survival and growth on microgreens. This work provides baseline data for risk assessment of microbial contamination of sprouts and microgreens. Understanding the risks of Salmonella contamination and its effects on rhizosphere microbial communities enables a better understanding of host-pathogen dynamics in sprouts and microgreens. The data also contribute to innovative preventive control strategies for Salmonella contamination of sprouts and microgreens.

Plant-microbe and abiotic factors influencing salmonella survival and growth on alfalfa sprouts and Swiss chard microgreens

16 February 2018

Applied and Environmental Microbiology, vol 84 no 9

Elizabeth ReedaChristina M. Ferreiraa, Rebecca BellaEric W. Browna and Jie Zhenga

doi:10.1128/AEM.02814-17

http://aem.asm.org/content/84/9/e02814-17.abstract?etoc

105 sickened, 1 death linked to Salmonella Newport outbreak originating in beef from dairy cattle, 2016-17

Contaminated ground beef was the likely source of a protracted outbreak of 106 Salmonella Newport infections, 42 hospitalizations, and one death in 21 states during October 2016–July 2017. While no direct link was found, whole genome sequencing suggests dairy cows were the ultimate outbreak source.

Foodborne outbreak investigations could be enhanced by improvements in the traceability of cows from their originating farms or sale barns, through slaughter and processing establishments, to ground beef sold to consumers.

In January 2017, the U.S. Centers for Disease Control (CDC) identified a cluster of Salmonella enterica serotype Newport infections with isolates sharing an indistinguishable pulsed-field gel electrophoresis (PFGE) pattern, JJPX01.0010 (pattern 10), through PulseNet, the national molecular subtyping network for foodborne disease surveillance. This report summarizes the investigation by CDC, state and local health and agriculture departments, and the U.S. Department of Agriculture’s Food Safety and Inspection Service (USDA-FSIS) and discusses the possible role of dairy cows as a reservoir for strains of Salmonella that persistently cause human illness. This investigation combined epidemiologic and whole genome sequencing (WGS) data to link the outbreak to contaminated ground beef; dairy cows were hypothesized to be the ultimate source of Salmonella contamination.

A case was defined as infection with Salmonella Newport with PFGE pattern 10 closely related to the outbreak strain by WGS, with bacterial isolation during October 1, 2016, through July 31, 2017. A total of 106 cases were identified in 21 states (Figure 1). Most illnesses ([72%]) were reported from southwestern states, including Arizona (30), California (25), New Mexico (14), and Texas (seven). Illness onset dates ranged from October 4, 2016, through July 19, 2017. Patients ranged in age from <1–88 years (median = 44 years), and 53 (50%) were female. Among 88 (83%) patients with known outcomes, 42 (48%) were hospitalized, and one died.

Initial interviews identified consumption of ground beef as a common exposure among patients. A focused questionnaire was developed to collect detailed information on ground beef exposure and to obtain shopper card information and receipts. Among 65 interviewed patients, 52 (80%) reported eating ground beef at home in the week before illness began. This percentage was significantly higher than the 2006–2007 FoodNet Population Survey, in which 40% of healthy persons reported eating ground beef at home in the week before they were interviewed (p<0.001) (1). Among the 52 patients who ate ground beef at home, 31 (60%) reported that they bought it or maybe bought it from multiple locations of two national grocery chains, and 21 (40%) reported that they bought ground beef from locations of 15 other grocery chains. Specific ground beef information was available for 35 patients. Among these, 15 (43%) purchased ground beef as chubs (rolls) of varying sizes (range = 2–10 lbs), 18 purchased it on a tray wrapped in plastic, and two purchased preformed hamburger patties. Twenty-nine patients reported that they bought fresh ground beef, four bought frozen ground beef, and four did not recall whether it was fresh or frozen when purchased. When asked about ground beef preparation, 12 (36%) of 33 patients reported that they definitely or possibly undercooked it.

Traceback Investigation

USDA-FSIS conducted traceback on ground beef purchased within 3 months of illness onset for 11 patients who provided shopper card records or receipts. Approximately 20 ground beef suppliers belonging to at least 10 corporations were identified; 10 of the 11 records traced back to five company A slaughter/processing establishments, seven of 11 traced back to five company B slaughter/processing establishments, and four of 11 traced back to two company C slaughter/processing establishments.

Product and Animal Testing

Opened, leftover samples of ground beef from three patients’ homes were collected for testing. All were purchased from one of two national grocery chains that had been identified by a majority of patients. One sample, collected from ground beef removed from its original packaging, yielded the outbreak strain. The other two samples did not yield Salmonella.

The outbreak strain was also isolated from four New Mexico dairy cattle. One was collected from a spontaneously aborted fetus in July 2016, and one was isolated from feces from a young calf in November 2016. The third isolate was identified by searching the USDA Animal and Plant Health Inspection Service National Veterinary Services Laboratory (USDA-APHIS NVSL) database for Salmonella Newport isolates collected from cattle in Arizona, California, Texas, New Mexico, and Wisconsin during January 2016–March 2017. Eighteen Salmonella Newport isolates were identified, including 13 from Texas, three from New Mexico, and two from Wisconsin. The only Salmonella Newport pattern 10 isolate identified was from a fecal sample from a New Mexico dairy cow collected during November 2016. The fourth isolate was from a USDA-FSIS routine cattle fecal sample collected at a Texas slaughter establishment in December 2016; USDA-FSIS determined the sample was from a dairy cow and identified the New Mexico farm of origin. Because of confidentiality practices, officials were not able to identify the farm or farms of origin for the dairy cows associated with the other three samples or whether the four dairy cows were associated with a single farm. None of the 11 patients with information for traceback ate ground beef produced at the Texas slaughter establishment.

Whole genome high-quality single nucleotide polymorphism (SNP) analysis* showed that 106 clinical isolates were closely related to each other genetically, to the four dairy cattle isolates, and to the leftover ground beef isolate (range = 0–12 SNP differences), suggesting that the Salmonella bacteria found in patients, ground beef, and dairy cattle all shared a common source. Thirty-nine additional clinical isolates with PFGE pattern 10 were determined to not be closely related and were excluded from the outbreak. No antibiotic resistance was detected among three clinical isolates tested by CDC’s National Antimicrobial Resistance Monitoring Laboratory.

Because the USDA-FSIS traceback investigation did not converge on a common production lot of ground beef or a single slaughter/processing establishment, and no ground beef in the original packaging yielded the outbreak strain, a recall of specific product was not requested. A public warning was not issued to consumers because specific, actionable information was not available (e.g., a specific brand or type of ground beef). Officials in New Mexico visited the dairy farm that was the source of the cow at the Texas establishment and noted no concerns about conditions or practices. However, this visit occurred late in the investigation, and conditions at the time of the visit might not have represented those present immediately before and during the outbreak. No samples from the environment or cows were collected during this visit.

Epidemiologic and laboratory evidence indicated that contaminated ground beef was the likely source of this protracted outbreak of Salmonella Newport infections. A significantly higher percentage of patients than expected ate ground beef at home, and a patient’s leftover ground beef yielded the outbreak strain. Dairy cows colonized or infected with the outbreak strain before slaughter are hypothesized to be the ultimate outbreak source. Most U.S. ground beef is produced from beef cattle; however, 18% is produced from dairy cows (2). Dairy cows are sold for beef production through sale barns or directly to slaughter establishments as they age or if their milk production is insufficient (2). Previous studies have demonstrated long-term persistence of Salmonella Newport in dairy herds (3,4), and a 1987 Salmonella Newport outbreak was linked to contaminated ground beef from slaughtered dairy cows (5). In the current outbreak, as has been observed in previous outbreaks, ground beef purchases traced back to numerous lots and slaughter/processing establishments (6). One possible explanation is that dairy cows carrying a high Salmonella load that overwhelmed antimicrobial interventions could have gone to multiple slaughter/processing establishments (7), resulting in contamination of multiple brands and lots of ground beef. This might explain the reason for failure to identify a single, specific source of contaminated ground beef.

This investigation identified the outbreak strain only in samples from dairy cattle from New Mexico. All four isolates from dairy cattle samples were closely related genetically by WGS to isolates from patients, providing further evidence of a connection between dairy cattle in New Mexico and the outbreak. The disproportionate geographic distribution of cases in the U.S. Southwest, including New Mexico, also suggests a possible regional outbreak source. Although limited in scope, the query of the USDA-APHIS NVSL data identified the outbreak strain only from one New Mexico dairy cow (isolate 3), and the sample collection date was consistent with the timing of illnesses in this outbreak. The overall prevalence and geographic distribution of the outbreak strain in cattle is not known, and it is possible that cattle in states other than New Mexico might have been infected or colonized with the outbreak strain.

This was a complex and challenging investigation for several reasons. First, the PFGE pattern in the outbreak was not uncommon in PulseNet, making it difficult to distinguish outbreak cases from sporadic illnesses associated with the same Salmonella Newport pattern. WGS analysis provided more discriminatory power to refine the outbreak case definition and excluded 39 cases of illness from the outbreak. However, sequencing is not currently performed in real time for Salmonella, thereby slowing the process of determining which cases were likely outbreak-associated. In addition, a direct pathway linking outbreak cases to dairy cows infected with the outbreak strain of Salmonella Newport could not be established. This is because product traceback did not converge on a single contaminated lot of ground beef, and investigators were unable to ascertain a link between the beef slaughter/processing establishments identified during traceback and the farms with dairy cows that yielded the outbreak strain. Tracing back ground beef purchased by patients to slaughter/processing establishments requires documentation such as receipts or shopper card records, and only 10% of patients had this information available. For this outbreak, tracing back cows at slaughter/processing establishments to the farm from which they originated was problematic because cows were not systematically tracked from farm to slaughter/processing establishments.

Four points along the “farm to fork” continuum provide opportunities to prevent consumers from becoming ill from contaminated ground beef. First, farms can implement good management practices for cattle health, including vaccination, biosecurity (e.g., controlling movement of persons and animals on farms, keeping a closed herd [so that no animals on the farm are purchased, loaned to other farms, or have contact with other animals], planning introduction of new animals and quarantining them, and performing microbiologic testing of animals), and cleaning and disinfection measures to decrease Salmonella burden in animals and the environments in which they reside, reducing the likelihood that Salmonella will enter beef slaughter/processing establishments (8). Second, slaughter/processing establishments are required to maintain Hazard Analysis and Critical Control Points systems to reduce Salmonella contamination as well as slaughter and sanitary dressing procedures to prevent carcass contamination (9). Third, although Salmonella is not considered an adulterant in not-ready-to eat (NRTE) meat products, USDA-FSIS likely will consider the product to be adulterated when NRTE meat products are associated with an outbreak (9). Finally, consumers are advised to cook ground beef to 160°F (71°C) as measured by a food thermometer to destroy any bacteria that might be present. Consumers are also advised to wash hands, utensils, and surfaces often; separate and not cross-contaminate foods; and refrigerate foods promptly and properly.

This investigation emphasizes the utility of WGS during outbreak investigations and identifies the need for improvements in traceability from the consumer to the farm. It also highlights the importance of continued evaluation of farm practices to help reduce persistent Salmonella contamination on farms, contamination of ground beef, and ultimately human illness.

Protracted outbreak of Salmonella Newport infections linked to ground beef: Possible role of Dairy Cows-21 states, 2016-2017

CDC

https://www.cdc.gov/mmwr/volumes/67/wr/mm6715a2.htm

Kis Robertson Hale, Food Safety and Inspection Service, U.S. Department of Agriculture; territorial, state, city, and county health departments and laboratories; Danya Alvarez, John Crandall, Hillary Berman-Watson, California Department of Public Health Microbial Diseases Laboratory.

 

The role of meat in foodborne disease

Meat has featured prominently as a source of foodborne disease and a public health concern. For about the past 20 years the risk management paradigm has dominated international thinking about food safety. Control through the supply chain is supported by risk management concepts, as the public health risk at the point of consumption becomes the accepted outcome-based measure.

Foodborne pathogens can be detected at several points in the supply chain and determining the source of where these pathogens arise and how they behave throughout meat production and processing are important parts of risk-based approaches. Recent improvements in molecular and genetic based technologies and data analysis for investigating source attribution and pathogen behaviour have enabled greater insights into how foodborne outbreaks occur and where controls can be implemented. These new approaches will improve our understanding of the role of meat in foodborne disease and are expected to have a significant impact on our understanding in the next few years.

The role of meat in foodborne disease: Is there a coming revolution in risk assessment and management?

Meat Science

Narelle Fega, Ian Jenson

https://doi.org/10.1016/j.meatsci.2018.04.018

https://www.sciencedirect.com/science/article/pii/S0309174018300731

Stop scamming in Spain: Crackdown on British tourists’ phony food poisoning

The British Ministry of Justice has announced new rules to stop British holidaymakers in Spain from scamming tour operators with fake food poisoning claims.

Under the crackdown, a limit will be set on the legal costs that can be claimed in overseas package travel claims. This will stop claims management companies from seeking legal costs that are out of proportion to the damages sought – a loophole that has often pushed tour operators to settle out of court.

In a press release, the Ministry of Justice said the change “would mean tour operators would pay prescribed costs depending on the value of the claim and length of proceedings, making defense costs predictable and assisting tour operators to challenge bogus claims.”

According to court documents, phony food poisoning claims may have cheated Spanish hotels out of as much as €60 million since 2014. The scam took off in the summer of 2016, with one hotel chain receiving 273 claims requesting compensation for 700 people.

The scam was simple enough. The tourist buys a travel package with any travel agent and stays at a Spanish hotel that includes all meals in the price. Back in Britain after the vacation, the tourist uses a claims-management company to file a complaint against the company that organized the trip, alleging that the hotel meals made him/her ill.

Current British consumer laws barely require the claimant to produce any evidence. No doctor’s report is necessary, and claims may be filed up to three years after the event.

Since it is hard to prove that the client did not get sick, and faced with high legal fees if the case goes to court, the tour operator accepts the claim, then pass on the cost to the Spanish hotels as per their contract, in which the latter accept responsibility for all damages.

In 2017, the Spanish Civil Guard arrested seven British nationals for their involvement in the scam.

According to the Association of British Travel Agents (ABTA), the number of claims jumped from 5,000 in 2013 to 35,000 in 2016 – an increase of 500%.

“Claiming compensation for being sick on holiday, when you haven’t been, is fraud,” said Justice Minister Rory Stewart. “This behavior also tarnishes the reputation of British people abroad. That is why we are introducing measures to crack down on those who engage in this dishonest practice.”

The Ministry of Justice says the new rules will come into effect shortly – well before summer begins.

In early April, a young couple who demanded compensation after claiming they fell ill on holidays were caught out thanks to their social media photos.

Chelsea Devine, 21, and Jamie Melling, 22, from Liverpool in the UK, went on a 10-day all-inclusive holiday to Benidorm, Spain in September 2015.

The holiday was booked with travel and tourism company TUI, and they stayed at the Levante Beach Apartments during their trip.

In May 2016, the couple both claimed they had contracted serious food poisoning from food and drinks consumed during their stay, and each demanded $4500 in compensation from TUI.

The pair claimed they were seriously ill during their holiday, and that the sickness lasted for weeks.

However, Liverpool County Court heard their social media accounts revealed a variety of happy, poolside selfies, which caused judge Sally Hatfield QC to brand them both as “fundamentally dishonest”.

They recently received a record fine of more than $27,000 for their fraudulent claim.

According to The Sun, Recorder Sally Hatfield QC said there was no evidence the pair had been ill during their trip.

In October 2017, UK couple Deborah Briton, 53, and Paul Roberts, 43, were jailed for making fake holiday sickness claims in a landmark case.

A foodborne illness outbreak could cost a restaurant millions, study suggests

A single foodborne outbreak could cost a restaurant millions of dollars in lost revenue, fines, lawsuits, legal fees, insurance premium increases, inspection costs and staff retraining, a new study from researchers at the Johns Hopkins Bloomberg School of Public Health suggests.

The findings, which will be published online on Apr. 16 in the journal Public Health Reports, are based on computer simulations that suggest a foodborne illness outbreak can have large, reverberating consequences regardless of the size of the restaurant and outbreak. According to the model, a fast food restaurant could incur anywhere from $4,000 for a single outbreak in which 5 people get sick (when there is no loss in revenue and no lawsuits, legal fees, or fines are incurred) to $1.9 million for a single outbreak in which 250 people get sick (when restaurants loose revenue and incur lawsuits, legal fees, and fines).

Americans eat out approximately five times per week, according to the National Restaurant Association. The Centers for Disease Control and Prevention (CDC) estimates that approximately 48 million people get sick, 128,000 are hospitalized and 3,000 die each year due to food-related illnesses, which are often referred to as food poisoning.

For the study, the researchers developed a computational simulation model to represent a single outbreak of a particular pathogen occurring at a restaurant. The model broke down results for four restaurant types: fast food, fast casual, casual and fine dining under various parameters (e.g., outbreak size, pathogen, and scenarios).

The model estimated costs of 15 foodborne pathogens that caused outbreaks in restaurants from 2010 – 2015 as reported by the CDC. Examples of the pathogens incorporated in the model were listeria, norovirus, hepatitis A, E. coli and salmonella. The model ran several different scenarios to determine the impact level ranging from smaller outbreaks that may incur few costs (i.e., no lawsuits and legal fees or fines) to larger outbreaks that incur a high amount of lawsuits and legal fees.

“Many restaurants may not realize how much even just a single foodborne illness outbreak can cost them and affect their bottom line,” says Bruce Y. Lee, MD, MBA, executive director of the Global Obesity Prevention Center (GOPC) at the Bloomberg School. “Paying for and implementing proper infection control measures should be viewed as an investment to avoid these costs which can top a million dollars. Knowing these costs can help restaurants know how much to invest in such safety measures.”

The research team found that a single outbreak of listeria in fast food and casual style restaurants could cost upwards of $2.5 million in meals lost per illness, lawsuits, legal fees, fines and higher insurance premiums for a 250-person outbreak. When looking at the same circumstances for fine dining restaurants, $2.6 million in costs were incurred. The subsequent costs of outbreaks can be major setbacks for restaurants and are sometime irreversible. For example, Chi-Chi’s restaurant went bankrupt and closed their doors in the U.S. and Canada permanently due to a hepatitis A outbreak in 2003. In the past decade, several national restaurant chains have lost significant business due to food-illness outbreaks.

“Even a small outbreak involving five to 10 people can have large ramifications for a restaurant,” says Sarah M. Bartsch, research associate at the Global Obesity Prevention Center and lead author of the study. “Many prevention measures can be simple, like implement adequate food safety staff training for all restaurant employees and apply sufficient sick leave policies, and can potentially avoid substantial costs in the event of an outbreak.”

Nanobot viruses tag and round up bacteria in food and water

A PR which continues with the we’re-all-hosts-on-a-viral-planet themed, but gives some advice about how to work with nature to achieve goals.

Viruses engineered into “nanobots” can find and separate bacteria from food or water.

These viruses, called bacteriophages or just phages, naturally latch onto bacteria to infect them (SN: 7/12/03, p. 26). By tweaking the phages’ DNA and decking them out with magnetic nanoparticles, researchers created a tool that could both corral bacteria and force them to reveal themselves. These modifications can boost the sensitivity and speed of rooting out bacteria in tainted food or water, the researchers reported March 20 at the annual meeting of the American Chemical Society.

“You’re taking the power of what evolution has done … to bind bacteria, and then we’re just helping that out a little bit,” said Sam Nugen, a food and biosystems engineer who leads the team designing these phages at Cornell University.

Competing technologies for detecting bacteria use antibodies, the product of an immune response. But these are expensive to produce and work best in a narrow temperature and pH range. In contrast, phages “exist everywhere,” making them potentially more broadly useful as bacteria hunters, Nugen said. “They’ve had to evolve to bind well in much broader conditions than antibodies.”

Phages identify and grab bacteria using proteins on their leglike tail fibers, which form a strong bond with compounds on the bacterial cell surface. To infect the cell, the phage injects its genetic material. This hijacks the cell, forcing its machinery to produce phage clones.

Nugen and collaborators programmed phages to tag E. coli bacteria. The team’s engineered phages contained extra DNA that told the bacteria to make an easily detectable enzyme. When the infection caused the bacterial cells to rupture and release the new phages, a chemical reaction involving the enzyme produced a measurable signal: light, color or an electric current. For example, the phages exposed E. coli in milk and orange juice by turning the liquids red or pink.

The researchers also loaded the phages with nanoparticles with a magnetic iron and cobalt core. Once the phages latched onto the bacteria, researchers could use a magnet to round the bacteria up even before the bacteria ruptured and announced their presence. This allowed the researchers to detect low concentrations of bacteria: less than 10 E. coli cells in half a cup of water. Conventional methods grow the bacteria into colonies to find them, which can take up to two days. But using the phages, Nugen and his colleagues skipped this step and found the cells within a few hours.

Using phages for magnetic separation would be “really nice for food and environmental samples because they tend to be really dirty,” said Michael Wiederoder, a bioengineer at the U.S. Army Natick Soldier Research, Development and Engineering Center in Massachusetts, who was not involved in the research. The salt, sugar and fats in food can slow the reactions of antibody-based tests, he said.

Also, the phages infect only bacteria that can reproduce, allowing testers to tell the difference between live cells and those killed by antibiotics, heat or chlorine. With food, “whether the bacteria are alive or dead is the difference between you getting sick and not,” Wiederoder said.

The nanobots could also prove useful for blood or other human samples. There, phages would provide a way to find resistant bacteria left alive after a course of antibiotics.

The next challenge: tinkering with the phages to tune which bacteria they go after. In nature, phages prey on specific species. But in food, it may be helpful to detect several common offenders, like E. coli, Salmonella and Listeria, or, alternatively, to have greater discrimination to find only the pathogenic E. coli and leave the rest.

We’re all hosts on a viral planet: Trillions upon trillions of viruses fall from the sky each day

When a stoned Carl Sagan used to do his TV bit and talk about billions and billions of galaxies, I turned my world inward, to the trillions and trillions of viruses.

I tell daughter Sorenne, I don’t care which you focus on, but get one of them right.

According to Jim Robbins of the New York Times, high in the Sierra Nevada mountains of Spain, an international team of researchers set out four buckets to gather a shower of viruses falling from the sky.

Scientists have surmised there is a stream of viruses circling the planet, above the planet’s weather systems but below the level of airline travel. Very little is known about this realm, and that’s why the number of deposited viruses stunned the team in Spain. Each day, they calculated, some 800 million viruses cascade onto every square meter of the planet.

Most of the globe-trotting viruses are swept into the air by sea spray, and lesser numbers arrive in dust storms.

“Unimpeded by friction with the surface of the Earth, you can travel great distances, and so intercontinental travel is quite easy” for viruses, said Curtis Suttle, a marine virologist at the University of British Columbia. “It wouldn’t be unusual to find things swept up in Africa being deposited in North America.”

The study by Dr. Suttle and his colleagues, published earlier this year in the International Society of Microbial Ecology Journal, was the first to count the number of viruses falling onto the planet. The research, though, is not designed to study influenza or other illnesses, but to get a better sense of the “virosphere,” the world of viruses on the planet.

Generally it’s assumed these viruses originate on the planet and are swept upward, but some researchers theorize that viruses actually may originate in the atmosphere. (There is a small group of researchers who believe viruses may even have come here from outer space, an idea known as panspermia.)

Whatever the case, viruses are the most abundant entities on the planet by far. While Dr. Suttle’s team found hundreds of millions of viruses in a square meter, they counted tens of millions of bacteria in the same space.

Mostly thought of as infectious agents, viruses are much more than that. It’s hard to overstate the central role that viruses play in the world: They’re essential to everything from our immune system to our gut microbiome, to the ecosystems on land and sea, to climate regulation and the evolution of all species. Viruses contain a vast diverse array of unknown genes — and spread them to other species.

Last year, three experts called for a new initiative to better understand viral ecology, especially as the planet changes. “Viruses modulate the function and evolution of all living things,” wrote Matthew B. Sullivan of Ohio State, Joshua Weitz of Georgia Tech, and Steven W. Wilhelm of the University of Tennessee. “But to what extent remains a mystery.”

We’re all hosts on a viral planet.

I didn’t understand this until fourth-year university, and it was only then I became interested in learning.

Until then, I was bored.

Researchers recently identified an ancient virus that inserted itDNA into the genomes of four-limbed animals that were human ancestors. That snippet of genetic code, called ARC, is part of the nervous system of modern humans and plays a role in human consciousness — nerve communication, memory formation and higher-order thinking. Between 40 percent and 80 percent of the human genome may be linked to ancient viral invasions.

Viruses and their prey are also big players in the world’s ecosystems. Much research now is aimed at factoring their processes into our understanding of how the planet works.

“If you could weigh all the living material in the oceans, 95 percent of it is stuff is you can’t see, and they are responsible for supplying half the oxygen on the planet,” Dr. Suttle said.

In laboratory experiments, he has filtered viruses out of seawater but left their prey, bacteria. When that happens, plankton in the water stop growing. That’s because when preying viruses infect and take out one species of microbe — they are very specific predators — they liberate nutrients in them, such as nitrogen, that feed other species of bacteria. In the same way, an elk killed by a wolf becomes food for ravens, coyotes and other species. As plankton grow, they take in carbon dioxide and create oxygen.

One study estimated that viruses in the ocean cause a trillion trillion infections every second, destroying some 20 percent of all bacterial cells in the sea daily.

Viruses help keep ecosystems in balance by changing the composition of microbial communities. As toxic algae blooms spread in the ocean, for example, they are brought to heel by a virus that attacks the algae and causes it to explode and die, ending the outbreak in as little as a day.

While some viruses and other organisms have evolved together and have achieved a kind of balance, an invasive virus can cause rapid, widespread changes and even lead to extinction.

 

Risk is not low if cause is not known: 5, then 19, now 34 sick and 1 dead sick in E. coli outbreak linked to Edmonton restaurant

If the E. coli-romaine lettuce made it to an Alaskan prison, maybe it made it to an Edmonton restaurant.

Just asking.

According to the Toronto Star, one person has died and more than 30 people have fallen ill following an E. coli outbreak that Alberta Health Services has called “extremely complex” to investigate.

In a statement, AHS says it has expanded its investigation into the source of an outbreak of E. coli, beyond cases directly linked to an Edmonton restaurant late last month.

While 21 of these lab-confirmed cases are linked to Mama Nita’s Binalot restaurant in Edmonton, AHS no longer has public health concerns related to the restaurant.

The number of lab-confirmed cases of E. coli has increased to 34, including 11 patients who have needed hospital care, and one patient who has died likely due to E. coli infection.

“This outbreak is extremely complex, however AHS, in partnership with other provincial and federal agencies, is doing all we can to protect the health of Albertans,” said Dr. Chris Sikora, a medical officer of health in the Edmonton zone, in a statement. “The risk of illness remains very low.”

AHS has not yet identified the source of these cases, but believes they are linked to the initial outbreak.

The risk is not low if the cause is not known.

AHS has worked closely with the owners of Mama Nita’s Binalot since it was identified that a cluster of people with lab-confirmed E. coli ate at the restaurant. AHS says the owners have taken significant steps to manage this issue, including voluntarily closing until AHS was confident the restaurant could reopen without presenting a risk to the public.