Daniel B. Cohen – Food Safety Website https://www.storkxx.com Breaking news for everyone's consumption Tue, 31 Jul 2018 01:27:13 +0000 en-US hourly 1 https://wordpress.org/?v=5.3.4&lxb_maple_bar_source=lxb_maple_bar_source https://www.storkxx.com/files/2018/05/cropped-siteicon-32x32.png Daniel B. Cohen – Food Safety Website https://www.storkxx.com 32 32 The New Country Doctor and the Clinical Diagnosis of the Farm https://www.storkxx.com/2013/12/the-new-country-doctor-and-the-clinical-diagnosis-of-the-farm/ https://www.storkxx.com/2013/12/the-new-country-doctor-and-the-clinical-diagnosis-of-the-farm/#comments Fri, 06 Dec 2013 01:23:34 +0000 http://www.storkxx.com/?p=81070 Continue Reading]]> A new kind of professional There are missing professions that would integrate epidemiology, farming and ecology. These are professions that would deal not just with existing human pathogens on-farm and in the rural environment, but with emerging pathogens and their control or prevention. They would cover the interaction of human pathogens with current microbial ecology, including plant and animal pathogens, and the dynamic evolution of pathogens as they flow to, through, and from the farm and rural environment. One example: In 2006-2007, I  proposed adding a new kind of medical/veterinary position to Cooperative Extension at Land Grant Colleges. I used the term Medical Extension Specialists. It was an example of one kind of new research professional engaged with human pathogens on-farm and in the farm environment. Although this received support from FDA (1) and from administrators at UC Davis, including the Western Institute for Food Safety and Security (WIFSS), as well as interest from the University of Wisconsin, the financial crisis in the fall of 2008 put an end to this kind of proposed innovation. At UC Davis, additional positions in Veterinary Medicine covered at least some of the same areas proposed for Medical Extension. The reasons for placing these research positions in Cooperative Extension will be discussed below. A second example would be the “new country doctor” of the title of this article. The meaning is reversed from the usual order: the patient is the country, countryside, farm, watershed or local ecosystem. The resonance of the usual meaning for country doctor is the same: a person who is engaged, informal, knowledgeable, perceptive and skilled. Beyond research there is practice. Like other doctors, the new country doctor would preferentially be more engaged with maintaining the health of a “patient,” such as a farm, or rural community. Both a traditional and a new country doctor would be concerned with human pathogens in the farm environment. The latter would be more concerned with the ecological dynamics of human pathogen movement between plants, animals and people, and, more specifically, with farming and other practices that prevent the introduction, establishment or development of new, worse human pathogens. The biological and economic health of farms and ranches for crop and animal production may also increasingly be dependent on understanding and enhancing the microbial ecology of farming and ranching. A new country doctor would have the opportunity to integrate new genomic knowledge and other tools with the complexities of farming in a rural ecology. It could be one of the most interesting professional occupations in which to engage. Emerging pathogens  The problem with emerging pathogens is not just that they represent new diseases to combat, or older diseases with new evil twists. It’s that they keep emerging. The older view was of a static situation: we win; the pathogens lose. Here is MacFarlane Burnet, 1962 (2):One can think of the middle of the twentieth century as the end of one of the most important social revolutions in history, the virtual elimination of the infectious disease as a significant factor in social life.” Burnet may have had in mind justifying his own new direction toward the immunology of cancers at a time when the only known infectious cause of cancer was in chickens (Rous sarcoma virus). One battle was won; on to the next one. It was a statement of confidence, if not of fact, and I think that confidence was general at the time: that the immunological, antibiotic and public health tools were available to control infectious diseases (3). Most of America, including farming and ranching, still lives in Burnet’s conceptual world. I should emphasize: not just farming and ranching. Otherwise, we would not have antibiotic soaps as common commercial goods, physicians would not prescribe antibiotics for viral diseases and, for clarity, we would call “antibiotics” antibacterials. It’s not just a problem of non-therapeutic antibiotic use in animal production, or apple growers wanting to use last-resort hospital antibiotics for control of bacterial plant pathogens such as fire blight (Erwinia spp., Enterobacteraceae (4a,b). This is still an active debate, in 2013). The history of the epidemiological response to new pathogens and pathogen evolution can be found in the Centers for Disease Control and Prevention’s initial issue of the journal Emerging Infectious Diseases. Two reviews start the issue, by David Satcher (5) and by Stephen S. Morse (6). Morse’s article is particularly relevant here because of its section on “Ecological Change and Agricultural Development” in human pathogen emergence:

“Ecological changes, including those due to agricultural or economic development, are among the most frequently identified factors in emergence. They are especially frequent as factors in outbreaks of previously unrecognized diseases with high case-fatality rates, which often turn out to be zoonotic introductions…. “Agricultural development, one of the most common ways in which people alter and interpose themselves into the environment, is often a factor. Hantaan virus … causes over 100,000 cases a year in China …. Conversion of grassland to maize cultivation favored a rodent that was the natural host for this virus, and human cases increased in proportion with expansion of maize agriculture …. “Perhaps most surprisingly, pandemic influenza appears to have an agricultural origin, integrated pig-duck farming in China …. “Because humans are important agents of ecological and environmental change, many of these factors are anthropogenic. Of course, this is not always the case, and natural environmental changes, such as climate or weather anomalies, can have the same effect.”

Note that the original epidemiological focus on farms and the farm environment was not concerned with food safety. Joshua Lederberg led the team from the National Academy of Science’s Institute of Medicine whose report in 1992 was the foundation for developing institutional responses to emerging infections (7). I did not see any mention of foodborne diseases there either. However, before it was decided to start a new CDC journal, there was briefly a new section in the CDC’s Morbidity and Mortality Weekly Report (MMWR). The April 16, 1993, issue started with an introduction describing a new series in MMWR on emerging infectious diseases. The first report in the new section was on the West Coast O157:H7 hamburger outbreak (8), where Jack-in-the-Box is referred to anonymously as “chain A.” In practice, emerging foodborne diseases were an issue from the beginning. It is easy to forget that finding the human pathogen O157:H7 as a non-pathogenic commensal in cattle was a shock. It was even more surprising to find O157:H7 in or on plants, starting with the apple cider and apple juice cases that were occurring around the same time as the Jack-in-the-Box outbreak (9). The interaction between human pathogens and plants has continued to be even more surprising, up until today. A brief survey of the research projects and publications of only three labs can illustrate this: Fred Ausubel’s lab at Harvard/Massachusetts General Hospital (10); Maria Brandl’s lab at USDA Albany, CA (11); and Ariena H.C. van Bruggen’s lab at the University of Florida’s Emerging Pathogens Institute (12). There are many others. A new country doctor, or a Medical Extension Specialist, would have to integrate veterinary, epidemiological, and ecological issues of pathogens, as well as the microbial interactions of healthy farm environments. The transition from Burnet’s world to a view of dynamic pathogen evolution and emerging infectious diseases seems difficult enough. For some years, there has been an attempt to create a paradigm shift  to integrate concepts of health and health disciplines “to obtain optimal health for people, animals and our environment.” The overall research program has often gone under the name of the One Health Initiative. The contributions of National Research Council and Institute of Medicine Reports on One Health are reviewed in the current issue of Emerging Infectious Diseases (December 2013) in an article by Carol Rubin, et al. (13). From a food safety perspective, “our environment” would include plants and crops, farms and the farm environment, and food production systems. The research seems to be ahead of the paradigm shift, but as a concept that might integrate at least some perspectives on farming and food safety with integrated epidemiological approaches, it seems like a welcome approach. It might at least provide a common language. I actually have higher hopes for integration of approaches in the farm environment and improving produce safety.   The clinical diagnosis of the farm “It takes three generations to grow a farmer.” (14) Farming, in this country, is a highly skilled and complex integrated occupation. It’s also high-risk, both physically and economically. Mitigating economic risk is a constant challenge. The complexity of farming is reflected in the need for 80 to 100 years worth of historical memory to intelligently guide decision-making. “A year like this one,” just in terms of weather, may most closely resemble a year in the late 1940s for farmers I work with in Eastern Washington. A particular combination of events – like a devastating fire at grain harvest – in my county, Yolo County, CA, may require going back to the 1920s. You may only live once, but over three or four generations, many rare combinations of circumstances have often occurred before. Farmers have to integrate complex data into practical decision-making and action, all the time, year after year. In order to integrate decisions about human pathogens in the farm environment, they need well-founded and well-researched, reliable information. They need people to work with who can help apply that information to the specific individual conditions of their farms and fields, crops and rotations, animals, and rangelands, soil types and climatic variations, ecologies and water sources. Cooperative Extension has been one of the most effective research and technology transfer agencies in the history of the United States. It was one of the integral parts of the success of the Land Grant colleges. The training and culture within Cooperative Extension is both (neutral) research and solution-oriented: problem-solving. They are not an enforcement agency. They can do excellent research. They can work with farmers. In California, we have been dependent on a small group of Extension Specialists for key field research on produce safety. Because the culture of an institution and profession is so important, we thought that Cooperative Extension was the best place to house Medical Extension Specialists as they developed their own approaches. Extension has been repeatedly decimated over the past 20 years. In states such as California, there are fewer than half the professional staff positions (county- and university-based) remaining. It is surprising that the Land Grants have not been able to do more to protect this key part of their mission, nor to use it as a model for technology transfer in other areas besides agriculture (15). It seemed important not to further this decline. Additional funding for new positions could possibly come from non-traditional sources, including Health and Human Services, EPA, and DHS, while maintaining or improving funding for agricultural extension. A new profession does not have to be university-based, but much of the training for a new profession will probably have to be. David Acheson, when at FDA, wrote about the positive impact this approach could have in medical education. In general, we thought that the starting place should be Land Grants that had both medical and veterinary schools and a strong foundation of epidemiology, microbiology and molecular biology. There is more to disease and ecology than is reflected in my own focus, which has been mainly on emerging bacterial human pathogens, because of the food outbreak record, and on bacterial and fungal infections/symbioses of plants. Protozoan and viral diseases sourced from U.S. farms have seemed secondary. This is obviously a limited perspective. One of my friends in the 1970s studied the increase in schistosomiasis following the concrete lining of irrigation ditches in Sri Lanka, and there are many such counter-intuitive results. I tend to leave out parasitology, and– if you will pardon the older expression – fauna. In designing a broader program of training, these kind of gaps should be corrected. What farmers need to increase food safety, more than regulations, are professionals who can carry out a clinical diagnosis of their farm. The goal is to maintain a dynamic equilibrium of healthy ecological interactions, to prevent human pathogen transmission, and to avoid new pathogen emergence. Developing and maintaining a healthy dynamic equilibrium is going to be different in a complex and rich ecosystem, and more attainable, than in a sterile or semi-sterile environment (16). In California, it is striking how many key researchers on human pathogens in the farm environment are in Veterinary Medicine and Veterinary Medicine Extension. This must reflect the continuing influence of the late Dr. Calvin W. Schwabe, who founded the first department of epidemiology in a veterinary school at UC Davis and worked to develop the integration of animal and human diseases, the one medicine concept, and the one health concept discussed above (17). UCD also has run an internationally oriented master’s degree program in Preventive Veterinary Medicine (18). One can imagine a number of different types of professional training that would be good disciplinary backgrounds for this new profession. My guess is that the first new country doctor will be a vet. (1) Letter from Assistant Commissioner for Food Safety Dr. David Acheson to the author, received Aug. 23, 2007. Besides supporting the new positions proposed for UC Davis, he commented on curricula effects in medical education: “We believe that education in agriculture and human health, foodborne pathogens and zoonotic diseases are essential components of medical school programs….”   (2) Quoted in James M. Hughes, Emerging Infectious Diseases: A CDC Perspective, 2001. Emerging Infectious Diseases, Volume 7, No. 3 Supplement, 494-496, June 2001. From: MacFarlane Burnet’s “Natural History of Infectious Diseases,” third edition, Cambridge University Press, 1962.  (3) Burnet would probably have been appalled at the continuing devastation of then known and existing diseases 60 years later, including cholera, infant diarrhea and a plenitude of parasitical diseases.  (4a) K.S. Bell, et al. 2004. Genome sequence of the enterobacterial phytopathogen Erwinia carotovora sussp. atroseptica and characterization of virulence factors. PNAS 101 (30): 11105-1110. Published online July 19, 2004.  (4b) T.H.M. Smitz, et al. 2010. Complete genome sequence of the fire blight pathogen Erwynia amylovora CFBP 1430 and comparison to other Erwinia spp. Molecular Plant-Microbe Interactions. MPMI, 23 (4) pages 384-393, 2010.  (5) David Satcher. 1995. Emerging infections: getting ahead of the curve. Emerging Infectious Diseases, Volume 1 (1), January-March 1995, pages 1-6.  (6) Stephen S. Morse. 1995. Factors in the emergence of infectious diseases. Emerging Infectious Diseases, Volume 1 (1),  January-March 1995, pages 7-15.  (7) Joshua Lederberg, et al. Emerging Infections, Microbial Threats to Health in the United States. Institute of Medicine. National Academy Press, Washington D.C., 1992. (8) Multiple authors, starting with M. Davis and C. Osaki of the Seattle-King County Department of Public Health.  Update: Multistate outbreak of Escherichia coli O157:H7 infections from hamburgers – Western United States, 1992-1993. MMWR, 42 (14), 258-262. April 19, 1993. (9) The hamburger outbreak overshadowed the May 1993 report in the Journal of the American Medical Association (JAMA) on hemolytic uremic syndrome (HUS) caused by drinking apple cider with O157:H7 in Massachusetts, and  similar cases in New York and Connecticut.   [R.E. Besser et al. An outbreak of diarrhea and hemolytic uremic syndrome from Escherichia coli O157:H7 in fresh pressed apple cider. JAMA 269 (17) 2217 – 2220. May 05, 1993.]  With hindsight, similar cases are probably traceable to the 1980s, including in Sacramento, CA, where the linkage between apple juice and HUS was made but not with pathogenic O157:H7. Similarly the Listeria monocytogenes 1981 Canadian outbreak was actually the first demonstration of foodborne listeriosis. [E.T. Ryser and E.H. Marth (editors). Listeria, Listeriosis and Food Safety, Third Edition. CRC Press, 2007 (page 94)].  Cabbage grown with raw and composted sheep manure, from a herd which had had listeriosis deaths, was made into coleslaw. Outbreaks traced to sprouts and lettuce in the 1990s and early 2000s continued to implicate fresh produce, as did the Odwalla (unpasteurized) juice O157:H7 outbreak. Finally, with the 2006 spinach outbreak, FDA had had enough, and human pathogens on leafy greens and other raw produce were unquestionably a national and regulatory issue. [FDA Statement on Foodborne E. coli O157:H7 Outbreak in Spinach. Oct. 06, 2006. See “Next Steps” section.  http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2006/ucm108761.htm ]. (10)  http://ausubellab.mgh.harvard.edu  (11)  http://www.ars.usda.gov/pandp/people/people.htm?personid=10920  (12)  http://www.epi.ufl.edu/?q=node/167  (13) Carol Rubin, et al., 2013. Review of Institute of Medicine and National Research Council Recommendations for One Health Initiative. Emerging Infectious Diseases, Volume 19, Number 12, pages 1913-1917. December 2013.  (14) This common saying seems to evade Internet search terms. “It takes three generations to make a farmer” is quoted in “The Promised Land” by Leavitt Ashley Knight, “Everybody’s Magazine” Volume 28, page 788, 1913. But this was a play on the more common “It takes three generations to make a gentleman.” I’ve heard it in the rural West for more than 35 years, and it was quoted (with “make”) by Oklahoma Labor Commissioner Mark Costello in 2012. (15) As an observation, the decline of Extension in CA seems to be in an inverse function to the number of university positions at the vice chancellor level and above. (16) One of the most protected and controlled medical environments is the hospital intensive care unit (ICU). Yet the control of methicillin-resistant Staphylococcus aureus (MRSA) and other multi-drug resistant organisms in ICUs is not only difficult but also the subject of considerable controversy on even the research results of control methods. See: K.T. Kavanagh, et al., 2013. A perspective on how the United States fell behind Northern Europe in the battle against methicillin-resistant Stapylococcus aureus. Antimicrobial Agents and Chemotherapy, volume 57, number 12, pages 5789-5791. December 2013. Published ahead of print, Oct. 7, 2013. The analogy in food safety is sprout production, also under the most protected and sealed environment imaginable, in this case for crop production, where pathogen introduction and spread is facilitated by the absence of any ecological controls of pathogens in a semi-sterile environment. Similarly, control of human pathogens in the crop phyllosphere (the above-ground aerial surface layers of plants) seems to be more difficult because of the reduced richness of plant surface ecology relative to soil and roots (rhizosphere ecology). Control systems still may be possible, but any biocontrol or beneficial microbial treatment is going to be much less well-buffered. (17) R.S. Nolan, 2013. Legends: the accidental epidemiologist. Dr. Calvin W. Schwabe fathered a generation of veterinary epidemiologists. JAMA News, July 01, 2013. Posted June 19, 2013. https://www.avma.org/News/JAVMANews/Pages/130701m.aspx  (18) http://www.vetmed.ucdavis.edu/mpvm/

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FDA's Proposed Produce Rule: A War on Farmers https://www.storkxx.com/2013/11/a-war-on-farmers/ https://www.storkxx.com/2013/11/a-war-on-farmers/#comments Wed, 13 Nov 2013 06:02:22 +0000 http://www.storkxx.com/?p=79657 Continue Reading]]>
The deadline for comments on the U.S. Food and Drug Administration’s Produce Safety Rule is Nov. 15, 2013. This was probably supposed to be the easiest and most straightforward of the rules to implement the Food Safety Modernization Act (FSMA). It may be that FDA fell into the trap of a well-worn groove in designing the Produce Rule. There are precedents for their approach from both Democratic and Republican administrations. However, this is the fourth time that manufacturers, processors and larger handlers of produce have attempted to use, or successfully used, food-safety legislation or state power to achieve multiple economic agendas – even when this would seem unnecessary, given their tremendous economic strength in the marketplace. In commenting on one of those attempts, I wrote: “It doesn’t take much time or experience to realize that Democrats act like they have never met a regulation that they didn’t like, and, if the regulation is ineffective, dysfunctional and complicated, they may like it even more. The Republicans claim they have never met a regulation they liked, except in practice, when it is demanded by an industry to give a gloss of procedural protection (biotech for example) or provides a barrier to competition protecting the largest companies in an industry from competition.” My view in this article is: a plague on both their corporatist houses. Different strands were contributed for different political reasons, but they were woven into a political, not a science-based, approach, which said that farmers are ultimately responsible for all produce safety problems; therefore, food safety is achieved by telling farmers what to do. Furthermore, that a farm can be treated in exactly the same way as an individual closed-system manufacturing plant, rather than recognizing the reality of farms being open to, and part of, both a larger polluted environment and a natural ecosystem – and often cooperating with other farms in a social agricultural community, or human ecosystem, if you like. It’s like blaming shellfish harvesters for the pollution entering Puget Sound, as well as the trucker who did not maintain a cold chain, the chain of stores that improperly stored the shellfish, and the ill restaurant worker who accidentally contaminated a seafood salad bar. What is more appropriate for regulating shellfish seems to be discourage  harvesting during the warmer months (those not spelled with Rs) , or when public health agencies detect concentrations of human pathogens. The three previous attempts to regulate produce, in this manner, were: (1) Use state power. This includes (a) the Leafy Green Marketing Agreements (first California, then Arizona) under the state equivalents of the 1937 Agricultural Marketing Agreement Act, creating industry-run state agencies under the Departments of Agriculture authorities; (b) the use of the federal law for the single-state (California) production of almonds under a mandatory Marketing Order, with a rule issued by the USDA’s Agricultural Marketing Service, and (c) changing a state law to incorporate food-safety practices for a commodity, which the Florida tomato industry did in 2008.
(2) Incorporate a national food-safety enabling section for produce marketing agreements and orders in the Farm Bill. (3) Create a national Federal Leafy Greens Marketing Agreement (or even Order), which is dormant but still pending. We are now on version (4), achieving similar goals under FDA’s proposed Produce Rules as an interpretation of FSMA. I was often quite naive about some of this. When the California Leafy Green Handlers Marketing Agreement was being implemented, the organizing procedures were being run by the chief counsel for the California Department of Food and Agriculture. He was a wonderful man who could have come straight from central casting and had to shepherd food corporation vice presidents into acting like a state agency. When I was trying to challenge him about the misuse and potentially illegitimate use of a progressive-era law to enable processors and handlers to regulate farmers (and not themselves) on food safety, he cut me off before I could finish the question because he thought he knew where I was going and said, “It’s not a problem. They are exempt from anti-trust under the specific language of the Act.” I hadn’t even considered anti-trust issues, but, sure enough, both the federal and state versions of the 1937 Acts (as amended) specifically exempt Market Orders and Market Agreements from anti-trust legislation and actions. What a deal! I found the food-safety theater aspects of FDA’s proposed Produce Rule on irrigation water quality, using indicator bacteria, to be an abysmal misuse of regulatory authority that would fail to enhance food safety except by accident, but would wipe out farms or eliminate major crops as options to be grown by many farmers. However, similar rules in the state programs also have a genuine legal and functional role. It shows a kind of science-inflected good will, which calms down the large buyers. It does not present the liability problems of having detected actual human pathogens like pathogenic Salmonella, O157:H7 and other pathogens in water (or other inputs) and, having documented this, potentially used the water (or other inputs). It’s better to be regulated by food-safety theater and not document intentional decision-making informed by genuine hazards; these may be dealt with in private. Here is another strand of the rope to hang farmers with:
The so-called Good Agricultural Practices, or GAPs, came in under the Clinton administration. I may be the only commenter who actively dislikes them. They were the soft-sell for “improving food safety on farms” by telling farmers what to do – without quite ordering them to follow other people’s guesses. As checklists of concerns, they can be useful. As specific demands for detailed practices, they can be worse than useless by giving a false sense of security to everyone. GAPs are not guarantees, even if they are treated roughly as guarantees in the marketing of produce. Global GAP Certification is a more rigorous and certified version of voluntary Good Agricultural Practices. A former secretary of the California Department of Food and Agriculture found his family-owned produce operation subject to a Salmonella detection recall (on peppers). The month before, they had been Global GAP Certified. The farm involved in the cantaloupe Listeria 2011 outbreak had received an extremely high rating from their third-party food-safety inspection. Litigation, liability, and now criminal liability adhere to actual contamination of food in commerce. How much of GAPs and certifications and inspections are just more food-safety theater? USDA and private groups did come up with a farm self-assessment food-safety software program, available from the USDA or FamilyFarmed.org, that may be more useful to some farmers than GAPs. A science-based question: Are there any studies documenting an improvement of safety after the implementation of the California LGMA? Answer: No. All right, then, are there any studies documenting that farms following GAPs and FDA Guidances improve food safety? Answer: No. FDA Guidances are hybrid animals. They are not regulations; farmers are not required to follow them, but not following them may increase potential liability. It’s not that GAPs and Guidances may not ever help. But the assumption behind assuming they will help is that farmers are not taking food safety seriously in the first place. Furthermore, the farmers who have already adopted following GAPs and Guidances may have done so to document food-safety practices they were already using in order to sell their produce to end-users. The difference in their food-safety concerns and practices before and after becoming GAP-certified may be nonexistent. Their ability to sell their produce, not their ability to implement food safety, may be the only change.
The assumptions behind the economic benefits to be derived from the FDA’s proposed Produce Rule are (approximately): “Farmers are idiots. Following the proposed Produce Rule will force them to improve their food-safety practices over an incompetent base level of inadequate food safety. Therefore, all food-safety practices, including those already used, including actual competent existing food-safety programs, can be counted as an economic benefit solely due to the proposed rule being implemented and to the supposed reduction in illnesses, all of which are accounted for as due to compliance with the Produce Rule.” Checklists are fine. Let’s recall that it was Curtis Lemay and a few other surviving top pilots who developed the aviation checklist so that the experimental planes that became the B-17 could safely be flown. Four of the best pilots in the Army Air Corps had just been killed or maimed in test flights. Safety checklists were developed by expert pilots that could protect every plane and crew before flight. Some 60 years later, similar checklists were developed by some hospitals for preventing respiratory infections in patients at risk after surgery, using the aviation industry as a model. I have never heard of a farm GAP or a produce Guidance whose development follows this model – where the persons with the greatest experience and competence, who have to implement, live with, and work with a safety program, design the program, hitting everything essential for survival. In this case, farmers with demonstrated expertise in both farming and delivering safe produce. There are major corporations that do this and small truck-farms that do this. Farmers have never run the farm food-safety agenda. You would think someone would notice, even as an academic observation. Enter the FDA, writing a Produce Rule implementing FSMA against this background. There seemed to be models, all of which claimed to be science-based produce-safety programs. Along with the models they were using, defective as these may or not be, they picked up some of the baggage that informed those models and came along for the ride. Briefly, this baggage includes: (a) the war on organics (still a cultural factor after all this time); (b) fear of competition from local production; (c) protection of the largest processors and handlers; (d) offloading as much liability and regulation as possible onto produce farmers; (e) disregarding systemic off-farm issues that affect farm safety, particularly urban waste streams and CAFOs. Therefore the proposed rules:
(a) Violate the specific language of FSMA, overriding the Organic Farming Production Act on compost and manure use and disregarding microbial ecological control of pathogenic micro-organisms. (b) Impose regulatory costs that will impact all farmers’ profits, but the largest farms the least harmfully, and, according to FDA’s own analysis, drive many farms out of business with complex facilities rules that will destroy food hubs and CSAs as common practices; (c) Neither regulate fresh-cut under the Produce Rule nor specifically regulate fresh-cut under any other rule (unlike sprout production); (d) Completely misuse food-safety statistics to imply, for example, that farming practices cause human-transmitted norovirus outbreaks or that amoebic contamination only found in foreign imports are due to U.S. farmers; (e) Fail to regulate inputs to farms from CAFOs, urban greenwaste, sewage sludge or ash, etc., according to their health hazards or risk before farm purchase. Some of the worst outbreaks in U.S. history have been the direct result of farmers or processors trying to improve food safety in handling on-farm or processing after delivery of raw produce. The farms and processors involved followed the advice of “the best and the brightest” to make their operations safer and ended up in disasters. Trying to improve food safety led to a food-safety failure. I am alone, perhaps, in finding that acquiring new equipment, including for specific food-safety reasons, or taking over old equipment new to a farmer or processor, is a specific hazard point that has to be controlled for. This can be made more dangerous when a farm or processor is expanding production and under market pressure to meet higher production levels. It seems to me to be obvious in the outbreak record. You might think that this record would result in a certain humility or caution in telling farmers exactly what to do, especially in those areas on which FDA’s expertise is most lacking, from planting to harvest. Yet this is exactly the area that the proposed Produce Rules spend most of their time on, with the greatest negative impact on farming and the fewest potential returns in actual improvement of food safety. The errors in the drafting of the Produce Rule propagate, populate and intensify in the other proposed rules implementing FSMA, including preventive control rules, foreign facilities, foreign imports, intentional contamination, third-party inspections, and others. Who among the congressional drafters of the legislation anticipated that the exceptions and exemptions for U.S. farmers under FSMA, such as the Tester amendment, would apply across borders to foreign producers with the same dollar values and distances? Yet that seems to be the interpretation.
Or that FDA would have no problem with sewage sludge for growing produce, so long as EPA’s complicated calculations on cumulative use are followed, and that this would open the door for importing foreign produce grown with sewage sludge for U.S. consumption (even if not legal for their own consumption)? Or that the failure to specify produce-caused outbreaks shall be a guide to drafting the Produce Rules would open the door to conflating outbreaks caused by farming practices (minimal in the record used), with handling and processing contamination (large), point of consumption (largest) and human-to-human transmission, all under the rubric of “FDA-regulated produce”? Most of the food processors I have met and worked with over the past 30 years are far more negative than I am about FDA’s role. One of my all-time favorite clients, a major West Coast food processor, could never refer to a former FDA commissioner – whom I liked – by his name, only by his full title: “That idiot, David Kessler, who thinks he knows more about running my business than I do.” It goes downhill from there. Actually, way downhill. Most farmers I have worked with are even more caustic about regulators. Some of them voted out the then-Speaker of the House when the Republicans gained control of the House. It goes downhill from there. And this is just the background farm culture. Few of them have had the pleasure of a uniformed FDA inspection by someone trained in regulating medical devices. Therefore, in my view, it is in FDA’s own interest to tear up the proposed Produce Rule and start again, aiming for statistical improvement in food safety by a few clear and simple rules that are not based on food-safety theater or corporatist favoritism, but instead follow FSMA’s direction in being actually science-based, that build on FDA’s existing strengths and competence, and are open to change with new information.
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FDA's Proposed Produce Rules Consistently Ignore Microbial Ecology https://www.storkxx.com/2013/10/cohens-third-fmsa-opinion-piece/ https://www.storkxx.com/2013/10/cohens-third-fmsa-opinion-piece/#comments Wed, 23 Oct 2013 05:03:47 +0000 http://www.storkxx.com/?p=78193 Continue Reading]]> An unnoticed side effect of the U.S. Food and Drug Administration’s (FDA) proposed Produce Rules will be the impact on the economics of large-scale animal production in the United States because they will be unable to dispose of their manures and litter off-site. Cattlemen, large chicken producers and other industry groups may have thought that rules on produce could not possibly affect them. FDA, however, in their notice of scoping for an Environmental Impact Statement (EIS) in the Federal Register, states (1a): “…Comments received caused FDA to reevaluate the proposed requirements for biological soil amendments of animal origin, which propose an increasingly stringent set of application restrictions based on the likelihood of the soil amendment harboring pathogens. These proposed requirements, if finalized, are expected to result in changes in current use of treated and untreated biological soil amendments of animal origin or potentially greater use of synthetic fertilizers. Changes in the type or handling of soil amendments may significantly affect the quality of the human environment.” This reason for an EIS comes from FDA’s peculiarly schizophrenic views on human pathogens in manures. Understandably concerned about contamination reaching produce – which can be consumed without a kill step – the agency takes the unusual step of preferring only expensive and energy-intensive chemical or physical sterilization for treatment of animal wastes. These require no waiting period after application on-farm. Then they recognize that sterilized manures and wastes are wide open for recontamination by human pathogens. As a consequence, sterilized composts, litters, or manures are potentially even more dangerous. The net result is they anticipate increased use of chemical fertilizer in conventional agriculture and leave large CAFOs (concentrated animal feeding operations) with a waste-disposal problem. Of course, composting is one of the several pathogen-reduction techniques allowed by the U.S. Environmental Protection Agency (EPA) for human waste, such as sewage sludge (biosolids), and the proposed Produce Rules have no problem with this use. Disregarding the explicit language of the Food Safety Modernization Act (FSMA), the proposed rules also impose new restrictions on organic farming, including a 45-day non-harvest period after applying compost. This includes composts that have been tested for O157:H7, salmonella, and indicator bacteria and documented before sale. As one organic farmer commented, “Why not just hold the compost an additional 45 days  before application if this actually had any value?” They also increase the waiting period after applying raw animal manures an additional four to five months (depending on crop) beyond the Organic Farming Production Act (OFPA). In a cynical reversal of congressional language and intent, FDA claims this is not a conflict: if farmers meet the new standard, they will also meet the old OFPA standard. FSMA language states the proposed rules should not cause changes in organic standards. Yet current organic farming laws and procedures of the National Organic Program (NOP), in general, have provided a much greater margin of safety for use of manures and composts than conventional agriculture. On the one hand, food safety across the country would be greatly increased if all farms followed the organic law for these soil amendments. On the other hand, the proposed changes would significantly harm organic farmers (see interviews with Tom Willey and Earthbound Farms in my comment on FDA’s proposed Produce Rule). A good compost is actively suppressive of human pathogens. This may seem surprising because usually the focus is on whether a compost has been made according to guidelines of carbon:nitrogen ratio, aeration, and other methodologies to guarantee high temperature generation for sufficient time to kill pathogens. If only exothermic, low energy, biologically generated heat sterilization were involved,  re-introduction of pathogens by contamination after cooling could allow pathogen regrowth. But this is just the first phase in composting. However, beginning with the cooling phase in compost development, the development of stable microbial diversity in mature composts can be suppressive of both human and plant pathogens when deliberately re-introduced (1b). Conversely, autoclaving mature compost and re-introducing human pathogens allows for pathogen survival and increase. In general, (2): “Contrary to the declining populations that are often seen in natural habitats, populations of E. coli can increase in such substrates under sterile conditions, that is, without predatory, antagonistic or competing organisms. This indicates that the natural microbiota in such cases has an overriding effect on survival.” The same can be true for soils (3), and plants, through their roots, can manipulate the soil ecology of the rhizosphere (4). The whole field is undergoing a major scientific revolution under the impact of  genomics and other biotechnologies. I would expect there to be major reviews and books on the molecular ecologies of farms and the interrelationship with human, animal and avian health in the near future as we learn to enhance beneficial microbial interactions at all levels. One of the major advances is that microbial populations can be characterized without having to be culturable, so a broader picture can be seen. Some examples include the detection of  native microbial populations that can suppress O157:H7 in dairy livestock bedding (5) and the detection of a native Salmonella-suppressant microbe that can be grown and used as a treatment in the production of tomato transplants and carry-over protection to the field in the southeastern United States. The latter came from research by Eric Brown of FDA’s CFSAN (Center for Food Safety and Applied Nutrition) division (6). The American Society of Microbiology recently published a free summary book on beneficial microbial interactions in agriculture (7). I interviewed two quite different people about this for my comment on FDA ‘s proposed Produce Rule (8). Tom Willey, with his wife Denesse, runs a 75-acre certified organic truck farm near Madera in California’s San Joaquin Valley. His farm relies on dairy compost from a well-established service that tests for O157:H7 and Salmonella, as well as for indicator pathogens.  They do not produce fresh-cut mixes or bagged produce because of the increased food-safety hazards. Will Daniels is vice president for food safety and organic integrity for Earthbound Farms, a major producer of bagged fresh-cut salads that handles more than 2 million pounds of produce per week. They run one of the most extensive microbial testing programs of inputs, produce received, and finished products before shipment I have ever heard of. Interestingly, they are in substantial agreement on using research-based ecological approaches to food safety. They also agree on an overall ecological and integrated approach to human, animal and plant health that respects and works with biological diversity, especially microbial diversity. How good are the composts that are commercially available? Tom Willey referred me to the only published study I have been able to find on microbial testing of commercial composts, noting it would not be pleasant reading. This is “Occurrence and Levels of Fecal Indicators and Pathogenic Bacteria in Market-Ready Recycled Organic Matter Composts” (9), a study submitted in early 2008 and published in 2009. The lead author, W.F. Brinton, Jr., has worked for years to develop the science and controls for composting, including the response to newly emerging pathogens such as O157:H7 (10 – 13). This study looked at point-of-sale commercial greenwaste composts produced in the three western states of Washington, Oregon and California. The authors were generally favorably impressed by the results because human pathogens were generally rare, although Salmonella was found in one compost. But they found a very wide range of fecal coliforms, and a slight majority of samples exceeded the EPA 503 standards. Furthermore, 6 percent of the samples had detectable O157:H7. A few years after the spinach crisis: “One facility produced compost with a very high fecal coliform level, and this facility was in a noted vegetable production area …. We detected measurable E. coli  O157:H7 in samples from three facilities. These facilities were in the large facility group and were situated within important vegetable growing regions.” Really bad composts were associated with exceeding the indicator bacteria levels even for Class B sewage sludge. Safer composts were correlated with windrowing compost methods, smaller facility size, and compost maturity as measured by the California Compost Maturity Index. “These data indicate that compost that is hygienic by common standards can be produced, but more effort is required to improve hygiene consistency in relation to management practices.” What is striking about this paper is that it was based on studying greenwaste, which is generally treated as safe for composting and use, including in FDA’s Proposed Rule. It did not take animal manure as a known input to create an unsafe compost. Some states allow a percentage of manure in greenwaste, but contamination can come from a range of practices in collecting urban greenwaste in particular. There are strong economic pressures to dispose of a range of waste products on agricultural lands. Urban sanitation systems, ash from biomass-based power plants, greenwaste to avoid landfill limitations, port and river dredging and CAFOs all are examples. All of them have an impact on food safety if they end up in farmland used for produce. But they are not all accurately managed for food safety. What about U.S. commercial manure-based composts? The best survey I have seen on this is a master’s thesis from Clemson University from 2011. Cortney M. Miller looked at 103 samples of organic fertilizers of various types, including manure compost, from nine states (collected from 2007 to 2010). The initial survey showed (14): “All of the organic fertilizer samples analyzed in this study were found to be free of Salmonella, E. coli O157:H7 and L. monocytogenes.” This may be classic risk-adjusted behavior. Knowing there is a potential hazard, the composters using manure (and other biological fertilizers) may be more careful than those using “only” greenwaste, which is assumed to be safe. If there were routine annual surveys of composts made from animal manures, state by state, method by method, and company by company, we would have useful data to work with and compare with similar surveys for greenwaste. But these data do not seem to be reported, if they are ever collected. Instead, there have been about 20 years of research papers on inoculating various soils, composts, and other inputs, as well as plants directly with known pathogens or their disabled surrogates, following their fate in the particular system, and this became the basis of various regulatory proposals or policy statements, including by FDA and the U.S. Centers for Disease Control (CDC). As few as 10 E. coli O157:H7 cells can be sufficient to cause a human infection (15). That is well worth being paranoid about or extremely careful. How many O157:H7 cells does it take to contaminate vegetables when the soil or growing media are contaminated by water or manure or compost? A typical set of papers by Islam et al (cited in the prologue to FDA’s proposed Produce Rule) looked at deliberately contaminated manure compost added to soil (or water) followed by growing leaf lettuce, parsley, carrots and green onions. “Pathogen concentrations were 10 to the 7th CFU/g [ten million cells/gram] of compost” (16, 17). For interest’s sake, what is the concentration of O157:H7 in the manure from a supershedder cattle? Supershedders are relatively rare individuals responsible for the majority of O157:H7 shedding from a herd of cattle. Sampling each animal’s own contamination levels in Angus, Brahman and Angus-Brahman breeds, Jeon et al. used the definition of more than 100,000 cells per gram – 10 to the 5th (18) for “supershedder.” Brahman cattle were highly resistant to carriage of O157:H7 compared to Angus and mixed Angus-Brahman breeds in this study. The normal range defining supershedders is above 1,000 to above 10,000 O157:H7 CFU per gram – 10 to the third to 10 to the fourth. Some reports have been as high as one million cells per gram – 10 to the sixth (19). Looking at the highest of these concentration numbers, it would be at least 10 times safer to grow vegetables directly in the manure of supershedder cattle than under the research experimental conditions. Johannesson et al. (20) gave an example of lower-level deliberate inoculation of O157:H7, not in compost but in dairy cattle manure and urine slurry. This was used as fertilizer one week before transplantation of crisphead lettuce (cv “Coquette”). This was at a level of “only” 10,000 (10 to the fourth) CFU/gram final soil concentration. “As the bacterium was not detected in the edible parts of the lettuce, the outer leaves of the lettuce, or the lettuce roots at harvest it was concluded that transmission of E. coli O157:H7 from contaminated soil to lettuce did not occur. The pathogen persisted in the soil for at least 8 weeks after fertilizing but was not detected after 12 weeks.” Interestingly, “Pseudomonas fluorescens, which inhibited growth of E. coli O157:H7 in vitro, was isolated from the rhizosphere.” A “good” soil can be suppressive of human (bacterial) pathogens. This seems to hold for Salmonella as well as O157:H7. There have been some great recent experiments on the possible contamination of tomato fruits from plants grown in pathogenic Salmonella(s)-contaminated drip irrigation water and for models of floral infection (splashing, overhead irrigation). Jie Zheng and co-authors were trying to prove the possibility of Salmonella surviving and infecting tomato fruits after a persistent outbreak of Salmonella (Salmonella enterica serovar Newport) on tomatoes on Virginia’s eastern shore (21). In this case, the outbreak strain was also found in a pond used for irrigation water, including when drip irrigation was used. Using a 100 million cell/ml root zone treatment, they were able to find one infected fruit, as well as persistence in stems. In contrast, blossom infection, presumably modeling  sprinkler irrigation or splash dispersal, was a much more facile route for fruit infection. So there is a possible pathway that suggests confirmation of the original outbreak investigation, and that even drip irrigation might be a possible pathway. However, as the authors point out, it’s also true that young transplants (with associated root wounding) were at a more susceptible stage – for any transport of Salmonella within the root or stem – and, in routine commercial field production, transplants were going into a routinely sterilized soil (under plastic). “… interior root colonization might occur passively through wounds in roots that are damaged during transplantation. Moreover, methyl bromide has had a long history of use in tomato cultivation as a soil fumigant in the eastern United States, and recent metagenomic studies have shown that such practices have diminished overall soil microbial diversity, perhaps increasing the potential for Salmonella colonization and persistence in the soil.” It takes introducing multiple risk factors to get Salmonella-contaminated water to infect a tomato fruit through contamination of roots. Risk could be mitigated in a number of ways to stop this, including a bacterial antagonist root drench at the end of transplant production in the greenhouse, possibly not sterilizing soil, and (of course) not using Salmonella-contaminated water for irrigation, particularly during the time window just before or after transplanting. Soil microbial ecology, or its absence, can be critical. Here is a trick question: How many cells of Salmonella does it take to contaminate a tomato fruit? No more than 100 cells, if one does it correctly, injecting directly into the peduncle of a young fruit. Unfortunately, Salmonella was able to thrive in this environment and grow to a density of 10 to the seventh per gram fresh weight of pulp. This was part of a University of Florida team’s experiment looking at what they called worst-case conditions for the contamination of tomato plants through above-ground parts (the phyllosphere, as opposed to the root-influenced zone in the soil, or rhizosphere). They also used a surfactant, Silwet L-77, to aid the contamination of leaves (leaflets) dipped into a solution of Salmonella enterica Typhimurium at a concentration of 10 to the ninth CFU per ml (one billion cells per milliliter) two to four times. They actually found internalization of Salmonella and movement to fruits, although rarely under these conditions. The authors argue that very low probability events, multiplied by the number of tomato plants commercially grown, show the possibility of this being an actual hazard. This is a slightly foolish justification for the research. Another way to look at it is: don’t sprinkler irrigate or surface irrigate with water contaminated with Salmonella at a concentration of one billion CFU per milliliter after spraying the field with surfactant. This would remove even the very low probability of occurrence through this route of contamination. The authors state that the practical implication of their work may be “… that application of surfactants, especially Silwet L-77, could enhance the entrance of bacterial pathogens into leaf tissues.” The more worrisome aspect is when a human pathogen and a plant pathogen synergistically aid each other (23): “The importance of phytobacteria in the persistence of human enteric pathogens on plants first came to light from supermarket produce surveys that demonstrated that 60 percent of produce showing symptoms of soft rot also harbored presumptive Salmonella …. Biotrophic plant pathogens, like P. syringae and Xanthomonas campestris, were also shown to promote growth or survival of Salmonella and enterohaemorrhagic E. coli on plants.” One of the soft rot pathogens, Dickeya dadantii (Erwinia chysanthemi 3937) is also a pathogen of the pea aphid (24). It’s a complex system. Internalization of a pathogen is the produce industry’s nightmare because no surface sanitization could even make a difference. Surface contamination seems to do the job of creating outbreaks perfectly well, however. If you put the studies together, you get what is becoming a common conclusion: while rhizosphere and soil microbial ecology systems can be well-buffered against pathogens, the phyllosphere or above-ground plant parts or edible portions are much more problematic, with much greater variability and much less stability than soil  and root ecological systems. And, of course, a research protocol using a sufficient concentration of a human pathogen, far beyond what one could expect on farms, can overwhelm the rhizosphere microbial ecology, often not measured or described in these studies. The potential ability of human pathogens to infect plants through flower parts, on the other hand, seems particularly troublesome. FDA did get one part of one aspect of this quite right, in my view. Any application to the above-ground portions of crop plants consumed raw should be evaluated for human pathogen issues of the water used. This includes pesticide applications, where human pathogens can use the pesticides themselves as energy sources (25), dust-control water, where the contaminated dust will then blow back onto growing fields after drying, and any other aerial application – as well as, of course, irrigation. Except for irrigation, these are inputs and sometimes professions (for example, pilots) where being part of the food-safety chain may not have been apparent. Modest awareness could bring large safety improvements, particularly when applications are close to time of harvest (26). FDA consistently ignored microbial ecology in drafting the proposed Produce Rules. In the case of above-ground plant parts, the phyllosphere, this happens to  have some justification – as a first approximation. In the case of soils, rhizosphere ecology, and soil amendments such as composts and manures, it leads them into a disastrous set of proposals. In the absence of comments from the animal industries, we have the curious situation that CAFOs may only be protected by the objections to the proposed Produce Rule from organic farmers and the sustainable agriculture community (27). FDA’s proposals, remarkably, would require the consumption of massive amounts of energy and cash to make manures and composts – and probably soils – more dangerous. References: (1a) Department of Health and Human Services, Federal Drug Administration. Notice of Intent to Prepare an Environmental Impact Statement for the Proposed Rule, Standards for Growing, Harvesting, Packing and Holding of Produce for Human Consumption. Federal Register, Vol. 78, No. 160. Monday, August 19, 2013 (pages 50358 – 50359). Proposed Rules. (1b) N. Paniel et al. 2010. Assessment of survival of Listeria monocytogenes, Salmonella Infantis and Enterococcus faecalis artificially inoculated into experimental waste or compost. Journal of Applied Microbiology, 108, 1797 – 1809. (2) van Elsas et al. 2011. Survival of Escherichia coli in the environment: fundamental and public health aspects. ISME Journal, 5, 173 – 183. (3) van Elsas et al. 2012. Microbial diversity determines the invasion of soil by a bacterial pathogen. [E. coli O157:H7].  PNAS January 24, 2012. 109 (4) 1159 – 1164. (4) Berendson  et al.  2012. The rhizosphere microbiome and plant health. Trends in Plant Science. August 20, 2012. 17 (8) 1360 – 1385). (5) Westphal et al. 2011. General suppression of Eschericia coli O157:H7 in sand-based dairy livestock bedding. Applied and Environmental Microbiology, March 2011, p 2113 – 2121. (6) Described in: Richard Coniff, 2013. Enlisting bacteria and fungi from the soil to support crop plants is a promising alternative to the heavy use of fertilizer and pesticides. Scientific AMerican, September 2013, p 76 – 79. (7)  Ann Reid and Hannon E. Gates. How Microbes Can Feed the World. Report on an American Academy of Microbiology Colloquium Washington DC // December 2012. American Society of Microbiology. August, 2013. See: HYPERLINK http://academy.asm.org/index.php/food-microbiology/5111-how-microbes-can-help-feed-the-world” http://academy.asm.org/index.php/food-microbiology/5111-how-microbes-can-help-feed-the-world (8) Daniel B. Cohen. Comment on: Standards for the Growing, Harvesting, Packing and Holding of Produce for Human Consumption. Proposed Rule Document issued by the Food and Drug Administration (FDA). Docket No. FDA-2011-N-0921 Regulatory Information Number RIN 0910-AG35. http://www.regulations.gov/#!documentDetail;D=FDA-2011-N-0921-0196 (9) Brinton et al. 2009. Occurrence and levels of fecal indicators and pathogenic bacteria in market-ready recycled organic matter composts. Journal of Food Protection, Vol. 72, No. 2, pp 332 – 339. (10) David Stip, 1991. “At Cafe Brinton, Today’s Special is Chicken a la Sawdust: the Julia Child of garbage cooks up tasty compost for the microbial palate”. The Wall Street Journal, Wednesday July 31, 1991. (11) Mary L. Droffner and William F. Brinton, 1995. Survival of E. coli and Salmonella populations in aerobic thermophile composts as measured with DNA gene probes. Zbl. Hyg. 197, pp 387 – 397. (12) William F. Brinton, 2000. Compost quality standards and guidelines. Final Report by WIlliam F. Brinton, Woods End Research Laboratory, December 2000. Prepared for: New York Association of Recyclers. (13) Brinton et al. 2005. Herbicide residues in composts: pH and salinity affect the growth of bioassay plants. Bull Environ Toxicol, November 2005. 75 (5) 929 – 936. (14). Cortney M. Miller, 2011. Microbiological safety of organic fertilizers used for produce. Thesis in partial fulfillment of the degree Master of Science, Microbiology.   (See page 44). (15) Y. Hara-Kudo and K. Takatori, 2010. Contamination level and ingestion dose of foodborne pathogens associated with infections. Epidemiology and Infection. Volume 139; Special Issue 10; October 2011, pp 1505 – 1510. (16)  M. Islam et al., 2004. Persistence of Enterohemorrhagic Eschrischia coli O157:H7 in soil and on leaf lettuce and parsley grown in fields treated with contaminated manure composts or irrigation water. Journal of Food Protection; 67 (7) pp 1365 – 1370. (17)  M. Islam et al., 2005. Survival of Escherischia coli O157:H7 in soil and on carrots and onions grown in fields treated with contaminated manure composts or irrigation water. Food Microbiology; 22(1) pp 63 – 70. January 2005. (18) Soo Jin Jeon et al., 2013. Evaluation of animal genetic and physiological factors that affect the prevalence of Escherichia coli O157:H7 in cattle. PLoS ONE 8 (2) e55728 (9 pages). (19) Elaine D. Berry and James E. Wells, 2010. Escherischia coli O157:H7: Recent advances in research on occurrence, transmission and control in cattle and the production environment. In Steve L. Taylor, editor: Advances in Food Nutrition Research, Vol. 60. Burlington Academic Press, 2010, pp 67 – 118. Elsevier. (20) Gro D. Johannessen et al., 2005. Potential uptake of Escherischia coli O157:H7 from organic manure and compost into crisphead lettuce. Applied and Environmental Microbiology; 71(5),  pp 2221 – 2225. May, 2005. (21)  Jie Zheng et al., 2013. Colonization and internalization of Salmonella enterica in tomato plants. Applied and Environmental Microbiology, 79 (8): pp 2494 – 2502. (22)  Ganyu Gu et al., 2011. Internal colonization of Salmonella enterica serovar Typimurium in tomato plants. PLoS ONE 6(11), e27340. (11 pages). (23) Maria T. Brandl et al., 2013. Salmonella interactions with plants and their associated microbiota. Phytopathology 103: 316 – 325. (24) Anne-Marie Grenier et al., 2006. The Phytopathogen Dickeya dadantii (Erwinia chrysanthemi 3937) Is a Pathogen of the Pea Aphid. Applied and Environmental Microbiology, 72 (3); pp 1956 – 1965. March, 2006. (25) Lopez-Velazco et al., 2013. Growth of Salmonella enterica in foliar pesticide solutions and its survival during field production and postharvest handling of fresh market tomato.  Journal of Applied Microbiology; 114 (5) pp 1547 – 1558. May, 2013. (26). See the interview with Scott Horsfall, CA LGMA in  Cohen 2013 (above). (27)  An alternative approach to FDA’s would be much more modest and limited to try and implement known steps that reduce hazards in produce. The current organic rules on composted manures, manure and sludge application are more protective than those for conventional agriculture. They could be adopted for all produce. This includes banning sewage sludge (“biosolids”) from produce production for multiple reasons, including non-pathogenic contaminants. FDA could regulate the commercial and other inputs to produce, rather than the farmers (or just the farmers). Manures and greenwaste could be tested for a range of human pathogens before they are even processed for farm application. The value of human pathogen-free manure or greenwaste should be higher in a free market because it will take less work to make them into a safe compost. The value of a pathogen-contaminated raw material should be lower. FDA could mandate testing of raw materials and let the market proceed. There could be improved consistent grading standards for composts. A good compost has no human (bacterial) pathogens. A great compost would be known to be human-pathogen suppressive. A perfect compost would be plant-pathogen suppressive and have killed any viable weed seeds to boot, but that is beyond the food-safety issues discussed here. FDA could regulate the government agencies that deliver water. The simplest regulation would be to notify farmers of dredging work that disturbs channel banks or bottoms and potentially releases pathogens. The more complex would be to mandate reporting of water quality to farmers by water agencies, not from farmers to FDA. A layered approach to produce safety in on-farm production has to include microbial ecology in soil amendments, composts, and, in fact, soils. The complexity of these ecological systems, and of farms and farmers, suggests that centralized management from a single rule and metrics applied everywhere – in the U.S. and for foreign produce – is guaranteed to fail. Working with farmers for improvements in safety, not an impossible guarantee of safety, is more likely to succeed. ]]> https://www.storkxx.com/2013/10/cohens-third-fmsa-opinion-piece/feed/ 3 FDA Barely Considers Biological, Chemical and Radiological Inputs in Proposed Produce Rule https://www.storkxx.com/2013/09/send-lawyers-guns-and-money-biological-chemical-and-radiological-inputs-to-produce/ https://www.storkxx.com/2013/09/send-lawyers-guns-and-money-biological-chemical-and-radiological-inputs-to-produce/#comments Thu, 26 Sep 2013 05:02:03 +0000 http://www.storkxx.com/?p=76836 Continue Reading]]>
Violating the explicit language of the Food Safety Modernization Act (FMSA), the Food and Drug Administration’s (FDA) Proposed Produce Rule gives a complete pass to imported vegetables grown with sewage sludge, contaminated to various degrees with heavy metals, polycyclic aromatic hydrocarbons, volatiles, flame retardants, pharmaceuticals, steroids, hormones (1,2) radiologicals (3) and undescribed contaminants. At the same time, the Proposed Rule makes it more difficult for U.S. organic farmers to use compost. It’s amazing.
FSMA states that the regulations are supposed to (4): “minimize the risk of serious health consequences and death… [with regulations to] prevent the introduction of known or reasonably foreseeable biological, chemical, and physical hazards, including hazards that occur naturally, may be unintentionally introduced, or may be intentionally introduced, including by acts of terrorism, into fruits and vegetables…” This sounds eminently reasonable. In my formal comment to FDA (5), I noted separate examples of radiological, chemical and heavy-metal contaminations that have taken farmland out of production within a few miles of where I live in Davis, CA. I also noted the increasing importance of urban farming. In cities such as Detroit, Milwaukee, Los Angeles and Boston, and, indeed, around the country, there is increasing use of land for produce production that has been heavily impacted by urban and manufacturing chemical hazards. North Carolina Cooperative Extension, for example, has a guide to avoiding hazards in urban soils (6). Will Allen of Growing Power, Inc., a Milwaukee-based Midwestern urban farming and community development project with a 20-year history, has the position that (7, and see 8): “…urban gardeners must grow their own soil, and use that soil to grow food.” Existing urban soil, he contends, is far too contaminated to risk growing food in. When you dig in urban areas, he says, ‘All you’re doing is stirring up lead, arsenic, all the bad guys in the soil. And the food takes up the contaminants.’” FDA’s Proposed Rule rather cavalierly dismisses chemical and radiological contamination issues, including heavy metals, and gives them barely any consideration in the 1,200-odd pages of supporting documents and discussions. In the prologue to the Rule, FDA states: “While we acknowledge the potential for chemical, physical or radiological contamination of produce, for reasons discussed in this proposed rule, we are not proposing specific standards for these hazards in this rulemaking.”
What are those reasons? “Illnesses attributable to chemical hazards are rare (Ref. 7). In fact, between 1997 and 2011, there have been no Class I recalls of produce associated with a chemical hazard for which there is a reasonable probability of causing serious health problems or death (Ref. 8). Current monitoring, regulations, and industry practice have been sufficient to keep these hazards under control.” This is the only place in FDA’s Proposed Rule discussions where the lack of a Class I recall record is used to justify non-regulation. Usually FDA only requires that a recall might be possible, sometime in the future perhaps, in order to justify regulation. The Reference 7, mentioned above, is an FDA “Memo to the File,” a very brief position statement that does not even mention heavy metals. It does note a famous 1985 aldicarb contamination of watermelons (which caused 1,175 illnesses), Three Mile Island and Fukushima, but says that other U.S. monitoring and statistical survey programs are enough protection to consumers against chemical, radiological and physical hazards (9). FDA appears to use an implicit standard of acute and immediate harm for “serious health consequences,” which I cannot find anywhere in the Food Safety Modernization Act. Cumulative, chronic or slow-acting heath threats are not discussed. Carcinogenic, mutagenic, and teratogenic hazards, among others, would be ignored, if this was applied consistently. The main assessment of risk is in the “Draft Qualitative Assessment of Risk to Public Health from On-Farm Contamination of Produce,” which still awaits peer review. This states, in a single footnote: “…our qualitative assessment of risk described in this document focuses on biological hazards only; the agency’s considerations related to chemical, physical, and radiological hazards are outside the scope of this assessment.” And, in Section IV of their introductory discussion of the Proposed Rule, FDA states that it tentatively concludes that the Proposed Rule should be limited to biological hazards. FDA eliminated any consideration of chemical, pesticide, heavy-metal and radiological hazards for the Proposed Rule. Considering these hazards might have identified a wide range of sources of environmental contamination needing some attention for produce production. These include contamination from mining, manufacturing, oil and gas production and urban wastes, for example. Sewage sludge is our canary in the coal mine on these issues because it can be brought directly to farms.
FDA has no problems even with the biological problems of sewage sludge in vegetable and fruit production and hands over any regulatory concerns to the complex existing Environmental Protection Agency rules. “§ 112.53 What prohibitions apply regarding use of human waste? “You may not use human waste for growing covered produce, except sewage sludge biosolids used in accordance with the requirements of 40 CFR part 503, subpart D, or equivalent regulatory requirements.” This refers to the famous (or infamous) EPA Part 503 (10) “Standards for the Use or Disposal of Sewage Sludge.” Subpart D covers a multitude of sins, including Class A sewage sludge, the cream of the crop, and Class B sewage sludge, the bottom of the barrel, so to speak. EPA makes no distinction between “agricultural lands” for, say, grain production and for fresh fruits and vegetables, or between food crop, feed crop, fiber crop, range land or pasture; it is all agricultural land. (Part D 503.11). FDA does not even mind raw sewage in produce production. In the prologue to the Rule, the agency says: “For example, if an untreated human waste (i.e., equivalent to domestic septage: “liquid or solid material removed from a septic tank, cesspool, portable toilet” (40 CFR § 503.9(f)), is applied to a field used to produce a food crop, then “Food crops with harvested parts that touch the sewage sludge/soil mixture and are totally above the land surface shall not be harvested for 14 months after application of sewage sludge” (40 CFR § 503.32(c)(1), cross-referencing § (b)(5) of the same section). We agree these standards are appropriate for protecting public health and, therefore, we are not proposing to implement further restrictions.” Contrast this with how the Organic Farming Production Act (OFPA) treats these issues in general (11): “The producer must manage plant and animal materials to maintain or improve soil organic matter content in a manner that does not contribute to contamination of crops, soil, or water by plant nutrients, pathogenic organisms, heavy metals, or residues of prohibited substances.” The Organic Farming Production Act has a simple and clear regulation on sewage sludge (12): “The producer must not use sewage sludge (biosolids) as defined in CFR 503.” This would have been a simple and enforceable rule for FDA to adopt for all produce.
Foreign production of fruits and vegetables that are imported into the United States has to meet the same or equivalent standards, as the U.S. rules,. FDA seems to have ignored the consequences for foreign production in its handling of sewage sludge. Since FDA proposes a low bar to use of sludge, one would expect foreign producers and governments to easily hop over that bar. They won’t have to petition for an alternative set of standards that are equivalent in safety. They can just use the U.S. produce regulations to justify sewage sludge in produce production for U.S. consumers, if not for their own consumers. Finally, there is a major issue of the interactions between chemicals and consequences for human health. Both David Acheson, in his Food Safety Website interview (13), and the National Research Council (14), in their 2002 review of EPA’s sludge rules (CFR 503) raise similar concerns. The levels set by EPA and others are done singly for each contaminant and source by source. But the human population is exposed to complex mixes of contaminants from multiple sources over extended periods of time. FDA’s Proposed Rule is silent on these issues as well. FDA focused on biological contamination. Did they do a good job on human pathogens in soil inputs to farms, at least? Unfortunately, no. They did not. There seems to be something else going on in the way the Proposed Rule is structured and in its analysis of relative risk and hazards of different inputs and practices. (1) U.S. Environmental Protection Agency. Biosolids: Targeted National Sewage Sludge Survey. EPA 822-R-08-014. http://water.epa.gov/scitech/wastetech/biosolids/tnsss-overview.cfm (2) U.S. Environmental Protection Agency. Final Response to the National Research Council Report: Report on Biosolids Applied to Land and the Results of the Review of Existing Sewage Sludge Regulations. December, 2003; EPA-822-F-03-010. (3) U.S. Nuclear Regulatory Commission. 10 CFR Part 20. Disposal of Radioactive Material by Release into Sanitary Sewer Systems; Withdrawal of Advance Notice of Rulemaking. Federal Register, Vol. 70, No. 217. Thursday, November 10, 2005. (4) USC Title 21 — Food and Drugs, Section 350h, Standards for Produce Safety (c) Criteria (1) In general, (A).
(5) Daniel B. Cohen. Comment on: Standards for the Growing, Harvesting, acking and Holding of Produce for Human Consumption. Proposed Rule Document issued by the Food and Drug Administration (FDA). Docket No. FDA-2011-N-0921 Regulatory Information Number RIN 0910-AG35. http://www.regulations.gov/#!documentDetail;D=FDA-2011-N-0921-0196
(6) CR Crozier, M Polizzotto and L Bradley. Soil Facts: Minimizing Risks of Soil Contaminants in Urban Gardens. North Carolina Cooperative Extension Service, http://www.soil.ncsu.edu/publications/Soilfacts/ AG-439-78_Urban_Soil_Contaminants.pdf (7) Will Allen: Growing Power and the Future of Food [event announcement and description]. Johns Hopkins Bloomberg School of Public Health. March 09, 2012. http://www.jhsph.edu/research/centers-and-institutes/johns-hopkins-center-for-a-livable- future/news_events/events/past_events/2012/will_allen.html (8) Growing Power, Inc. Website: http://www.growingpower.org (9) Nega Beru. Memo on Chemical, Physical and Radiological Hazards Associated with Produce. Memorandum for the Record. Department of Health and Human Services, Public Health Service, Food and Drug Administration. May 29, 2012. (10) Code of Federal Regulations, Title 40, Part 503, http://www.gpo.gov/fdsys/pkg/CFR-2012-title40-vol31/xml/CFR-2012-title40-vol31- part503.xml#seqnum503.11 (11) The Organic Foods Production Act of 1990 (OFPA), 7 U.S.C. Section 6501, et. seq., as amended, is implemented in 7 CFR Part 205, the NOP Final Rule, which regulates the production, handling, processing, and labeling of all raw or processed agricultural products to be sold, labeled, or represented as organic in the United States. The quote is from § 205.203(c). (12) 7 CFR § 205.203 (e) (2). (13) James Andrews. IAFP 2013: Interview with Keynote Speaker Dr. David Acheson. Food Safety Website. Aug. 06, 2013. http://www.storkxx.com/2013/08/iafp-2013-interview-with-keynote-speaker-dr- david-acheson/#.Ujnb6ha6hz8

(14) Committee on Toxicants and Pathogens in Biosolids Applied to Land, National Research Council. Biosolids Applied to Land: Advancing Standards and Practices. The National Academies Press, National Academy of Science. 2002.

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FDA's Proposed Produce Rule is 'Food-Safety Theater' https://www.storkxx.com/2013/09/wading-in-the-irrigation-waters-fdas-proposed-produce-rule/ https://www.storkxx.com/2013/09/wading-in-the-irrigation-waters-fdas-proposed-produce-rule/#comments Tue, 10 Sep 2013 05:03:19 +0000 http://www.storkxx.com/?p=75778 Continue Reading]]> The U.S. Food and Drug Administration’s Proposed Produce Rule is a substantively defective product. It’s not a question of the difficulty and costs of compliance and enforcement or of farm size or a commodity’s inherent safety – although these are important issues. The case I want to present is that FDA made seriously wrong choices on too many issues: irrigation water standards; biological inputs such as compost, radiological and chemical hazards; sprout production and fresh-cut production; epidemiological data and economic analysis. Like other hazardous and defective products, the Proposed Rule should be recalled. Today’s column is about irrigation water. Here is the relevant section of the Proposed Rule for testing water: “Article 112.44 (c) When agricultural water is used during growing activities for covered produce (other than sprouts) using a direct water application method you must test the quality of water in accordance with one of the appropriate analytical methods in subpart N. If you find that there is more than 235 colony forming units (CFU) (or most probable number (MPN), as appropriate) generic E. coli per 100 mL for any single sample or a rolling geometric mean (n=5) of more than 126 CFU (or MPN, as appropriate) per 100 mL of water, you must immediately discontinue use of that source of agricultural water and/or its distribution system for the uses described in this paragraph. Before you may use the water source and/or distribution system again for the uses described in this paragraph, you must either re-inspect the entire agricultural water system under your control, identify any conditions that are reasonably likely to introduce known or reasonably foreseeable hazards into or onto covered produce or food-contact surfaces, make necessary changes, and retest the water to determine if your changes were effective; or treat the water in accordance with the requirements of § 112.43.” I hope that’s clear. Farmers are supposed to be able to follow the Food Safety Modernization Act without being forced to hire consultants or private certifiers. Note that there are precise and enforceable – and, as we shall see, useless – metric standards such as “126 CFU per 100 ml” (in a rolling geometric mean) of generic E. coli. The problem is that the generic E. coli standard is completely uncorrelated with the human pathogens of concern that have caused produce outbreaks and recalls such as E. coli O157:H7 and Salmonella. Worse, it has been shown to be uncorrelated with these human pathogens in actual production of leafy greens and other produce in numerous published studies, including by researchers from USDA and UC Davis, for California production, and by other researchers across the country. The largest data set, however, is from a California fresh-cut processor whom I interviewed as part of writing a comment on the Rule. For more than six years, they have tested about 2 million pounds of produce a week, as well as the farm inputs used to grow those 2 million pounds. They tested both for specific human pathogens, such as Salmonella and O157:H7 E. coli, and for generic E. coli, which is required for members of the California Leafy Green Handlers Marketing Agreement (CA LGMA). Their summary: the generic E. coli standard can be exceeded without human pathogens being present, and it can be met when human pathogens are actually present in high quantities. It is not a useful standard for produce safety. Trevor Suslow, in a Pew Issue Brief (1), described the origins of this standard and accurately predicted its increased use: “A limited, and arguably outdated, set of indicators of fecal contamination has been used by the fresh produce industry to assess the suitability of water used in preharvest crop production up to the point of harvest. Many regional GAP and CSG systems have relatively recently adopted EPA recreational water quality criteria for establishing action thresholds, in the absence of actual risk-based data based on irrigation water…. As internal and external pressure is exerted for national standards, a simple approach has been to adopt these EPA criteria.” The standard the FDA proposes to enforce on farmers, as federal regulation, is derived from a now-superseded U.S. Environmental Protection Agency (EPA) analysis and recommendation to state and tribal health authorities for recreational water. The EPA criteria were developed for a different purpose than produce safety and in a different context. This recommendation, and its successor published in the Congressional Record in November 2012 (2), is designed to prevent an excessive number of gastrointestinal illnesses for swimmers, such as 32 illnesses per thousand persons swimming in an ocean or fresh water body of water. The choice of generic E. coli (one of two standards to be met) is based on the actual correlations between epidemiological data on illnesses after swimming and measured indicator organisms. Generic E. coli  (along with Enterococci) had the most robust correlation with actual GI illnesses for fresh-water recreational use out of all the indicators of (mainly) human fecal contamination that were looked at. Looking at the update 2012 EPA Recreational Water Quality Criteria (3) and consistent with the previous standard: “Viruses are thought to be the etiologic agent responsible for most of the GI illnesses that are contracted in recreational waters impacted by sources of human fecal contamination….” Generic E. coli bacteria are used as an indicator of fecal contamination to correlate with largely viral GI illnesses, not for identifying the bacterial pathogens that have caused most produce outbreaks, serious illnesses or deaths (nor with more serious viral illnesses). The original group to adopt the recreational swimming standard and generic E. coli as the indicator species and metric was the CA LGMA. They had their own reasons and context for this choice. One was that, for all its problems, they found that using other bacterial indicators of  fecal contamination were actually worse standards. Generic E. coli was the best of a bad lot of indicators, for their purposes. To my surprise, I found on interview that there has never been a study of the effectiveness of the LGMA in preventing outbreaks. I suspect the same is true for the related GAPS programs. FDA itself never reported conducting an assessment of the efficacy of any of these programs before adopting their metrics or standards as models. It never even got to the level of evaluating the context, role and effectiveness of the irrigation water standard. It gets a little worse. A USDA team reviewed “Irrigation Waters as a Source of Pathogenic Microorganisms in Produce” in 2011 (4). They found: “Despite the general belief that irrigation water poses a potential source of pathogens in food-borne outbreaks, there are relatively few confirmed cases in the USA.” Most of the surface waters of the United States will fail the generic E. coli standard either persistently, predictably during certain times of the year or intermittently. This is a problem for most farmers who want to irrigate. Due to the peculiarities of the proposed rule, however, farmers using buried drip for irrigation and their own controlled wells as a source of irrigation will have an easier time complying. Commercial bulb onion producers were among the first to comment on the irrigation standards (5). One production and irrigation region in Oregon and Idaho, which produces about 20 percent of U.S. onions, would have to cease onion production under the metrics of this rule (6). The possibility of generic E. coli levels in irrigation water stopping irrigation and therefore killing a crop would prevent farmers from ever receiving a production loan, long before even considering “treating” the water of a 750,000-acre irrigation system. On the other side of the country, in Pennsylvania, an interesting two-year study of smaller farms with multiple types of surface-water sources for irrigation found that many farms would fail the generic E. coli tests, although O157:H7 and Salmonella were not detected and while Salmonella could be found occasionally when irrigation water would have passed the tests. It also showed that how samples were chilled and iced for transport to an accepted laboratory could greatly affect results and, therefore, consequences of the testing (7). The problems with surface-water irrigation, identified in early comments, are one of the two reasons that FDA now has called for a full environmental review (EIS) rather than stating the Proposed Rule is categorically exempt (8). The concern is not with the standards, however. Instead, FDA anticipates that so many farmers will switch to well irrigation, despite the expense, that it may affect the status of fragile aquifers. When the basic standard itself is problematic, all the rest of the regulatory requirements around that standard look very strange. Farmers will have to follow a sampling program that tells them how often they should test using a meaningless standard. They will have to document that they have sampled according to the frequency protocols for the meaningless standard. They will also have to document the results of their useless sampling so they can demonstrate to an inspecting authority that their irrigation water passed the meaningless standard. There are very exact protocols that must be followed. Overall compliance costs (not just for irrigation) are a high percentage of operating profits, but failing the meaningless standards for irrigation could be economically devastating. FDA added an extra (and almost sadistic) twist. Farmers can be faced with an entire crop being lost because they have to stop irrigating when irrigation water fails the standard. They have the option of treating their irrigation water with a chemical to kill pathogens. This chemical must, however, be EPA-approved for treatment of irrigation water. There are no such EPA-approved chemicals. There are no EPA standards for testing chemicals to be used to kill pathogens in irrigation water. EPA has no plans, currently, to develop such a standard. A chemical that can kill human pathogens could also wreak havoc with soil microbial ecosystems, farm by farm, in entire irrigation systems and across the nation. FDA’s solution is to delay implementation of the irrigation-water standard by two years. My conclusion on irrigation-water regulation is that FDA will be bankrupting farmers, driving them out of business, preventing new farmers from entering, and shipping produce production out of the United States, and without enhancing food safety. What we will get, instead, is food-safety theater. References: (1) Trevor V. Suslow. Standards for Irrigation and Foliar Contact Water. Produce Safety Project Issue Brief. An Initiative of the Pew Charitable Trusts at Georgetown University, 2010. (2) Environmental Protection Agency. 2012 Recreational Water Quality Criteria. Federal Register, Vol. 77, No. 230; Thursday, November 29, 2012, Notices (pages 71191-71192). Notice of availability and recommendations. (3) Environmental Protection Agency. Recreational Water Quality Criteria (RWQC). Office of Water 820-F-12-058. 2012. (4) Yakov Pechepsky, et al. Irrigation Waters as a Source of Pathogenic Microorganisms in Produce: A Review. Advances in Agronomy, Vol. 113 pp 73-138. 2011. (5) National Onion Association. Comment from the Dry Onion Industry Regarding FDA’s Proposed Rules… (Docket No. FDA-2011-N-0921). Docket for the Proposed Produce Safety Rule, Comments, May 2013. (6) Sean Ellis. “Water Quality Rules Unleash Flood of Fear: Proposed regulations could bring an end to PNW onion crop.” Capital Press [Agricultural Newspaper]. Updated: Saturday, July 06, 2013, 12:11 AM. (7) Audrey Draper. Microbial survey of Pennsylvania water used for specialty crop irrigation and development of sampling, handling and shipping procedures for surface water testing. MS Thesis, Food Science, Pennsylvania State University. December, 2012. (8) Department of Health and Human Services, Federal Drug Administration. Notice of Intent to Prepare an Environmental Impact Statement for the Proposed Rule, Standards for Growing, Harvesting, Packing and Holding of Produce for Human Consumption. Federal Register, Vol. 78, No. 160. Monday, August 19, 2013 (pages 50358-50359). Proposed Rules.   ]]> https://www.storkxx.com/2013/09/wading-in-the-irrigation-waters-fdas-proposed-produce-rule/feed/ 12 Produce Farming on the Brink https://www.storkxx.com/2012/03/produce-farming-on-the-brink/ https://www.storkxx.com/2012/03/produce-farming-on-the-brink/#respond Mon, 05 Mar 2012 09:59:07 +0000 http://foodsafetynews.default.wp.marler.lexblog.com/2012/03/05/produce_farming_on_the_brink/ Continue Reading]]> Our process of framing and regulating produce food safety is upside down and backwards.


Human pathogens constantly flow from urban environments and animal production into farm environments, contaminating water and soil, and finding a home in wildlife. Then we ask farmers to deliver pathogen-free fruits and vegetables.

Produce is increasingly sold as centrally processed fresh-cut products, diced fruits and cut salads in wholesale and retail packages, facilitating cross-contamination without a kill step. Then it is shipped in closed plastic containers that can allow pathogen maintenance and growth, with use-by dates of about three weeks from harvest. A cold chain for processing and delivery, that prevents E. coli O157:H7, for example, from multiplying allows Listeria to survive or thrive.

On farm, two of the greatest hazards have nothing to do with actually growing the crop. Washing, cooling and storage — on-farm handling, and providing sanitary conditions for employees that do not lead to human-to-produce contamination. On farm regulation focuses on field practices.

Farmers are asked to cut down trees and shrubs, which provide habitat for birds; to fence off fields and water sources, which might attract deer and other large species; to bury poisoned bait stations around the perimeters of their field, to prevent squirrels, mice, shrews and other rodents from entering their fields; to remove the low-growing filter strips next to streams, which actually prevent fertilizer run-off and some pathogens from entering the streams, because they also attract wildlife.

They are supposed to have management practices that prevent flies and other insects, snails and other invertebrates, frogs and other amphibians, from carrying human pathogens onto their fields. All have been shown to be potential carriers. Since farm food safety is focused on growing operations, sources that provide human pathogens to contaminate the fauna of a farm ecosystem are not regulated.

I use produce outbreaks where there have been outbreak investigation reports as case studies that provide some, limited, evidence. They may or may not support this thesis. They provide a window into how produce safety is being framed and understood.

In this article two of the 2011 outbreaks are covered: the Jensen Farm Listeria-cantaloupe outbreak and the Jaquith Farms O157:H7 strawberry outbreak. The implications for food safety policy are covered on the national and then small-farm scales.


Using the normal rules of thumb that make sense of food safety, there should never have been a Jensen Farms lLsteria cantaloupe outbreak. We may be in a changed world.

The FDA environmental assessment Report (1) states:

“This is the first listeriosis outbreak associated with a whole fruit or vegetable raw agri- cultural commodity. Listeria monocytogenes contamination has historically been associ- ated with ready-to-eat and processed food products, such as deli meat, unpasteurized cheese, raw milk, fresh-cut fruit, and fresh-cut vegetables, and is typically thought of as an environmental contaminant of food plants. Known reservoirs for Listeria monocytogenes include ruminant animals (e.g., cattle, goats, and deer), decaying vegetation, and cold, wet, and difficult to clean environments.”

Fresh-cut fruits and fresh-cut vegetables are recent food additions to the list. The usual combination of concern is Salmonella and cantaloupes, not Listeria,

With 33 deaths out of 146 reported cases, the Listeria-cantaloupe outbreak was one of the worst foodborne outbreaks in over 80 years. The death rate is close to 25 percent.

In many outbreak investigation reports I have read, “absence of evidence” in a processing facility is taken to be “evidence of absence,” even when it was documented that management had spent up to a week sanitizing their plant post-outbreak and pre-inspection.

In the Jensen Farms case, the equipment design and facility design prevented sanitation, both before the outbreak and before the investigation. Outbreak strains were found within the packing facility and cold storage. It was a rare case of presence of evidence, and some equipment had to actually be cut out and replaced in order to be sanitized to show no Listeria.

When the FDA looked for a source of contamination on-farm, they took the more usual approach.

“All environmental samples collected in the growing fields were negative for Listeria monocytogenes.”

Despite this:

“FDA has determined that the growing environment cannot be eliminated as a potential contributor in the introduction of Listeria monocytogenes contamination…”

That is true, as far as it goes, but it is also true of pretty much every farm in the country, given the ubiquity of ruminants and of Listeria in the environment. It does not do much to explain the origins or root cause of this unique case (2).

Many observers, including Bill Marler, have characterized the on-farm handling as gross negligence; and condemned the lack of prevention by food safety auditors. Jensen Farms had passed its audits for safety. Its papers were in order.

Now Jensen Farms appeared to me to be a large or very large operation responsible for a national outbreak centered on Colorado and Texas. Based on the recalled canta-Jim loupes alone, it looked like it probably was one of the 5,600 largest farms in the country with farm gate sales of over $5 million.

Jim Prevor had outstanding coverage of the outbreak in his Perishable Pundit articles but with a very different perspective (3):

“If Wal-Mart really put food safety first, it would have never bought cantaloupes from this small producer, which produced in a six-week season what California ships in a day.”

A small farm with local production, and small farms are not safe? We do not seem to be talking about the same outbreak. When I asked him about this, it turned out we were using the same words with different meanings from different contexts (4).

Prevor’s context is the national produce market, dominated by the largest buyers and their major produce suppliers. The vocabulary of the buyers is different than farmers, and perhaps most of their customers. “Local” can be defined as “within a 7 hour drive” by Whole Foods. “Small” in this world of the top strata within the top 5,600 farmers (the number is for all crops, not just produce) includes Jensen Farms. He estimated that maybe 10 of the very large melon farms in the U.S. had the money, size and motivation for a particular kind of food-safety processing equipment.

His main point was that the largest buyers do not make food safety their first priority in buying decisions, when one looks at how they actually operate. For example, if they can label produce as “local,” in their terms, this can have top priority. Buying from a “small” farm like Jensen Farms may meet a marketing decision for “local” produce, despite there being major farms with better food safety capacity. Therefore “safe versus local” as a choice. He was using the words as industry terms; to people outside the industry, they read differently.

Prevor then makes a critical observation: that how major produce buyers are actually rewarded determines the effectiveness of food safety commitments. He wrote an interesting analysis of overall food safety issues, including changing liability so that food safety is not unrewarded (5). On a national policy level his
approach and mine have many points in common. Trying to use common language:

The food system as a whole should be evaluated by a hazard analysis. The worst hazards overall should have the highest priority for being dealt with.

To really have an effective outbreak, one has to have a way to spread and multiply the pathogens; incidental contamination won’t do the job.

Any centralized source for contaminating produce, which spreads, multiplies, and preserves pathogens is more dangerous than any incidental source. Handling and processing can be major centralized sources in handling, and fresh-cut is a special hazard in part because it is food processing without a kill step.

Widespread hazards from the farm environment also can create broadly contaminated produce, for example from contaminated surface water or ground water or flooding.

Within farming operations, handling operations, packing and cold storage as in Jensen Farms, might be the highest priority after water quality and direct exposure to feces. Texas may be the state that has gotten this right, with a new law focused on on-farm handling (and processing).

Incentives for individual decision makers also can determine over-all food safety. Company incentives for major buyers are also a critical control point for food safety. Business expansion and growth with increased contracted deliveries can be a hazard for two reasons: newly acquired equipment can be a hazard, and pressure to deliver can lead to pressure on safety standards (6).

However, right now, we are quite distant from this approach.

On October 06, 2006, as the spinach outbreak was ending, the FDA put out one of the bluntest statements issued by a bureaucracy, saying to the lettuce and spinach industry that enough was enough, clean up your act or we will do it for you; and inadvertently creating the category of “leafy greens” (7).

In my view, what happened next was a tactically brilliant takeover by the major processors and handlers of the produce safety issue, starting with the California LGMA. It left farmers under the control of processors, who somehow left out the food safety issues of handling and processing operations.

The fundamental flaw in this approach is that in the absence of an effective kill step, for fresh-cut in particular, they basically have to sterilize the farm environment instead, which is impossible. It can be an ecological, social and strategic disaster. [For detailed discussions of the impact on farm environments see the Wild Farm Alliance website (8).]

This “processor-favoring” approach dominates all discussions of food safety on farms.

A cold-hearted analysis of sprouts as a commodity, that takes food safety as the first priority, is that they should be cooked. A cold-hearted analysis of fresh-cut as a commodity is that it is a food safety failure. We could go back to local production consumed within a few days of harvest for salad greens; local food service doing their own cutting for “fresh-cut” fruits and vegetables. This eliminates the pathogen increase time from farm to retail to consumption, and other factors. As commodities, both sprouts and fresh-cut lack kill steps and provide humid sealed environments in plastic containers for pathogen maintenance and increase.

Food safety, looked at cold-heartedly, is not the top priority when fresh-cut processing is analyzed. Other factors, including market share, value-added, and consumer convenience are priorities. Priorities have to be balanced, perhaps. It is not a justification for displacing all food safety concerns onto farms.

That still leaves the whole produce outbreaks.

It’s curious. No one studies the effectiveness of small farms at achieving food safety. I once heard an FDA hearing commissioner explain to an audience of mainly large processors and grower-shippers: “what you call a spinach harvester, I call a pathogen inoculator.” Harvesting on small farms is completely different, but which techniques are better or worse for food safety in comparison?

Can small farms really have a better safety record, and if so why; due to which practices?

The 2011 E. coli O157:H7 outbreak in Oregon involving Jaquith Strawberry Farm, initially thought to be a small grower, looks like a fairly large producer, distributing through multiple channels. One of them, Ron Spada Farms, was reported to have recalled 4,800 flats still in inventory after the outbreak trace-back. Other strawberries went to roadside stands, farm stands and farmers markets as if they were self-produced (9).

This can make “knowing your farmer” problematic. The farmer wasn’t small, and the people who looked like small farmers weren’t farmers, or had not grown the crop. Consumers may have had the illusion they were buying from a small local farmers in many parts of Oregon. Only the epidemiological trace-back found the common source.

There was no complete outbreak investigation report, but the outbreak strain was found in deer feces in the actual sole-farm’s strawberry production field. If there is a widespread pathogen contamination of deer, it did not affect multiple producers.

UC Davis field studies showed that O157:H7 in deer in California was quite rare, challenging the frequently made association with some California outbreaks. Oregon might be different.

There are many actual small strawberry producers in Oregon. They all managed to avoid causing outbreaks. There also are very large producers (super-farms) including Driscoll’s, which appears to have an outstanding food safety record, who also grew and sold strawberries safely.

It looks like this outbreak could have been due to negligence, probably at harvest, on one “medium” sized farm; that ordinary precautions might have been enough to prevent contamination even with the presence of E. coli O157:H7 in local deer.

Is there a statistical distribution of food safety by farm size? We know that the pressure of growth can be a major hazard point, throughout the produce outbreak record. Food safety can slip under the pressure to meet increased sales.

Actual incentives are not just a hazard point for the largest national produce buyers; they can compromise safety priorities for individuals or operations anywhere in the supply chain.

This outbreak involved multiple illnesses and one death. It was a relatively local, perhaps “regional” and “limited” outbreak. That is cold or no comfort to the family of the person who died or to those who became ill.

One can imagine a consensus on a set of national priorities focused on fixing the worst hazards first, an FDA that puts more emphasis on causal analysis of outbreaks as Michael Taylor has called for, and co-management of food safety and the preservation of habitats and the farm environment, as both the California LGMA and the Wild Farm Alliance have called for. Overall food safety would be greatly improved.

That is not where we are, right now.

What can I say to a small organic farmer who asked me about the impact of the three major outbreaks in 2011, and the oncoming regulations under the Food Safety Modernization Act (FSMA)?

By acreage, she and her husband are small farmers under any U.S. definition, owning and farming 20 acres. By farm gate sales they are in the top 20 percent of U.S. farmers.

Something like this:

Most of the work being done on food safety is not for their benefit and the regulatory schemes in process may be mostly harmful, imposing burdens without improving overall food safety because it avoids dealing with major hazards in the overall system of food production.

Regulators have a compulsive belief in the efficacy of complex paperwork, almost for its own sake. It could be called faith-based paperwork. The same money could be spent on solving problems, but they assume the solutions are all known.

In contrast, they should try and align their ordinary commercial records with food safety, an approach also favored by some major food safety consultants for the largest firms.

They need to know how to approach a recall, and be able to trace-up deliveries quickly.

Regulation will be based on the largest farms, even when these have been the source of multiple recalls or even outbreaks. Systemic failures such as the Listeria-cantaloupe case will not lead to new systemic approaches.

Expect to pay for third-party audits that lack meaning; and Extension services, which might have been helpful in actually solving safety problems, have been cut in half.

Reduce known hazards. There may be some crops, and some ways of growing and harvesting crops, that have to be dropped. Look carefully at washing, handling and packing.

Make food safety an over-riding contingency of sale in delivery contracts. Make food safety a part of any plan to grow production and sales, from the start. Consider increasingliability insurance and buying business interruption insurance.

Improved safety, and meeting all imposed regulations, provides no legal protections. In- cidental contamination beyond farmer control still comes under strict liability.

They can improve their odds.

I can guess that the ethical standards they use in all their approaches to farming do have a beneficial impact on food safety as well, for their size of farm, because they frame their own personal incentives, and oppose temptations to cut safety to meet a dellivery.

“Don’t screw up.” Know the common important hazards and have a systematic plan to control their risks.

You are always,farming on the brink of disaster.

(1) Environmental Assessment: Factors Potentially Contributing to the Contamination of Fresh Whole Cantaloupe Implicated in a Multi-State Outbreak of Listeriosis October 19, 2011

(2) A lot of specific information is missing from the report that could be useful in analyzing the outbreak and preventing future outbreaks. Jensen Farms used equipment that could not be cleaned, that came from a non-cantaloupe use (supposedly for potatoes). Was the previous operation contaminated with the outbreak strains? Similarly, a truck was used to bring culls to a cattle operation as feed and could have been a contaminant source for the cleaning and packing facility. Were outbreak strains found in the cattle operation? A neighboring field was reported to have received municipal sewage sludge, of unreported treatment, and Listeria bacteria are resistant to degradation in sludge. It would be important to know if the outbreak strains were found in the neighboring field.

I read ” All environmental samples collected in the growing fields were negative…” in a lawyerly fashion, and wonder why environmental samples collected in the larger environment were not reported on.

For a comprehensive review of Listeria and food safety and Listeria in the agricultural environment see, for example: Listeria, Listeriosis, and Food Safety, Third Edition

Edited by: Elliot T. Ryser, Michigan State University, East Lansing, USA; Elmer H. Marth, University of Wisconsin, Madison, USA March 27, 2007 CRC Press

(3) Perishable Pundit: The Cantaloupe Crisis: The Truth That Dare Not Speak Its Name: The Priority Can Be Safe Or The Priority Can Be Local, But It Cannot Be Both , October 4, 2011

(4) Perishable Pundit: “A Choice Had To Be Made: Which Was The Top Priority: Buying Cheap, Buying Regional Or Buying Safe?”

(5) Jim Prevor “How to Improve Food Safety” The New Atlantis, May 21, 2010

(6) For example, that is my reading of the outbreak reports for two major cases: Odwalla juice, and Dole spinach, as well as others.

(7) FDA Statement on Foodborne E. coli O157:H7 Outbreak in Spinach, October 06, 2006.

See “Next Steps” section.

(8) http://www.wildfarmalliance.org/

(9) Deer Confirmed as Source of Strawberry Outbreak  August 18, 2011, Food Safety Website


Daniel B. Cohen is the owner of Maccabee Seed Co., an agricultural research-and-development and consulting company in Davis, CA. See also “Sizing Food Safety Regulations to Fit the Farm” and “An Outbreak Like Germany’s Could Happen Here”

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An Outbreak Like Germany’s Could Happen Here https://www.storkxx.com/2012/03/an-outbreak-like-germanys-could-happen-here/ https://www.storkxx.com/2012/03/an-outbreak-like-germanys-could-happen-here/#respond Fri, 02 Mar 2012 01:59:07 +0000 http://foodsafetynews.default.wp.marler.lexblog.com/2012/03/02/an_outbreak_like_germanys_could_happen_here/ Continue Reading]]> I am interested in how major foodborne outbreaks and their investigations are interpreted and analyzed: to prevent future outbreaks, minimize the harm from outbreaks that occur, and frame the debates on regulating food safety on farms.

When I was asked by a small organic farmer in California what the implications were of the 2011 O104:H4 European outbreak, I said it could happen here. It also could have worse consequences here.

Let’s review the O104:H4 outbreak conclusions:

In Germany there were nearly 4,000 cases, 54 deaths and 845 cases of hemolytic uremic syndrome (HUS) — unusually, mainly in adults (1) (2).

One hundred percent of the German O104:H4 cases were associated with the production of fenugreek sprouts on a single organic farm in Lower Saxony, with regional distribution centered on Hamburg. The organic farm was found to have satisfactory sanitation and proce- dures and is back in operation.

The epidemiological evidence indicates that a particular lot of fenugreek seed, sold from or produced in Egypt, had become contaminated with this highly unusual outbreak strain. The same outbreak strain was associated with a secondary outbreak in France, also linked to fenugreek sprouts from the same seed lot, but produced as children’s projects and served at a local festival.

Where it starts getting more complicated is that sampling for O104:H4 found no positive results from fenugreek seed lots. There also were no positive results from tens of thousands of environmental samples taken during the post-outbreak investigation, although contaminated sewage and streams were found during the outbreak period. The conclusion was that much better culturing methods were needed for tracking the environmental presence of this pathogen.

Partially confirming data on O104:H4 having a regional origin comes from European tourists, who have become infected with related, but not identical O104:H4 strains after trips to Turkey, Egypt, Tunesia and Afghanistan (3). This supports the idea of regional endemic sources of O104:H4, but not where and how the fenugreek seeds were actually contaminated.

The Egyptian Ministry of Agriculture strongly objected to the identification of Egyptian seeds as the outbreak source in the absence of positive detection of the outbreak strain.

That is where things stand now, with clear identification of the food carrier and the source farm, but with some ambiguity as to the ultimate root cause of the outbreak and the specific mechanism of contamination.

The primary role for epidemiologists and public health officials during a foodborne outbreak, like the O104:H4 outbreak in Germany and France, is to stop the epidemic. If  an intervention stops the outbreak, then the identification of the cause is verified. Identification is based on epidemiological evidence; and direct detection is a kind of luxury of evidence. The tools they use have been developed primarily for this purpose, and may be less useful in determining other aspects, such as the search for confirmation of root causes and mechanisms of contamination.

How did the context in Germany shape the investigation and outcome in ways that might be different from the U.S.?

When O104:H4 infections hit Germany, the first “vegetables of interest” were E. coli-contaminated organic cucumbers from Spain, revealed publicly before there was confirmation that the E. coli did not match the outbreak strain. This was curious because of the lack of any outbreak — O104:H4 or other — due to the same two suppliers in Spain itself. Not that any pathogen finding is good, but at least one of the sources was told his cucumbers were seen spilled on the ground at the Hamburg Central Produce market. Perhaps even the non-outbreak pathogens were not due to the farm source. Spanish farmers and the Spanish government saw this as lingering prejudice against Spain.

European Union and German payments were later made to partially compensate Spanish growers.

In contrast, as far as I can tell, there have been no EU lawsuits against the farm for the actual outbreak. So what would be a strict liability case in the U.S. appears to be neither negligence nor foreseeable under the German equivalent law.

There were at least two cultural presumptions, also different in Germany from the U.S. that may reinforce this. Organic appears to be regarded as naturally safer, to the point where the Health Minister was quoted as saying “Of course we know that organic is not really safer.” And fenugreek sprouts were part of a common elaborated sprout cuisine in which sprouts are perceived as a natural healthy food.

U.S. epidemiologists seemed stunned that raw sprouts were not on the top of the list for food surveys in the case/control studies, given the outbreak histories for sprouts. German epidemiologists initially thought including sprouts would only create false positives in case/control studies because sprouts, in general, are so common a food item.

A CDC-FDA-state investigation of a similar outbreak here in the United States would focus more quickly on sprouts given the long history of sprout outbreaks. But perhaps the greatest difference in attitudes is toward organic farming.

Why should Europeans perceive organic farming as safer than conventional agriculture? A substantive reason is that the rules elaborated for organic animal production may provide better protections against transmission of human pathogens, both in the U.S. and the EU. Here I will use U.S. examples.

The Organic Foods Production Act (OFPA), passed in 1990, created the National Organic Program (NOP). Labeling was the basis of the law, that food be correctly identified as organic, but that was the hook for protecting the word “organic” and defining the farming practices.

The U.S. rules for organic compost, in an abundance of caution, were based on EPA guidelines for the use of human waste. This was supposed to provide a wide margin of safety for the use of animal manures. In many studies of E. coli O157:H7 or surrogate pathogen survival under these rules, undertaken since the spinach crisis, it appears that there is a margin of safety even for these STEC but it is not particularly wide.

Organic rules prevented the re-feeding of waste meats from slaughter, including brains and nervous tissue, long before mad cow (BSE) emerged, They ban the non-therapeutic use of antibiotics. They ban the use of dried cow manure as dairy bedding. They require more adequate space for animals and birds so that, for example, de-beaking of chickens is not allowed, or needed due to the insanity produced in birds from overcrowding in a stimulus- deprived environment. The overcrowding of birds, or cattle in CAFOs, may facilitate disease transmission and therefore, in some CAFOs, the routine use of antibiotics, but there also are ranchers who buy antibiotics by the multi-gallon tote without confining their cattle. Most antibiotic sales (by volume) are for animal use in agriculture, between 70 – 80 percent (4).

Organic rules ban the re-use of manures as animal feed.

Last summer, when I was working with a “medium-sized” organic vegetable producer, the price of composted chicken litter (for organic fertilizer) had gone through the roof because of increased demand for pelleted chicken litter in cattle feeding. Thanks in part to the California Leafy Green Marketing Agreement rules, at least there is now research interest in how exactly to p
asteurize different manures for conventional agriculture [for Salmonella, see (5)].

Since it is not an obvious step to feed brains or manure back to cattle, where did this come from? As far as I can tell, many of the changes in conventional animal production after World War II were driven by economists looking for efficiencies in production, without considering biology. They looked at the nitrogen content of manure, for example, and saw inefficiencies in cattle digestion (!) which could be re-captured, rather than fertilizer for soils (6).

All of these factors had to be specifically banned in organic animal production either be- cause they were once routine, or still are routine, in U.S. conventional agriculture. They all could play a role not only in the transmission of human pathogens but in the selection and evolution of more dangerous pathogens: by multiplying and spreading pathogens in closed biological systems, by acting as selection systems for antibiotic resistance and increased tolerance of acidity and other stresses, and by favoring selection for lateral transmission of groups of pathogenicity traits between pathogen species.

Even when there is an underlying substantive basis, EU positive attitudes toward organics may be due more to complex cultural attitudes than to substance.

Food safety criticisms of organic that I hear or read in the U.S. are often based on a failure to understand that most agricultural manures go into conventional agriculture, and for decades only organic agriculture had rules that were specifically designed to prevent human pathogen transmission (7). There is nothing to prevent conventional agriculture from using similar approaches, and sometimes there is a convergence toward safety.

What are some contrasts we could expect in a similar outbreak in the U.S.?

U.S. epidemiologists might identify a sprout-caused outbreak more quickly, and limit the duration of the outbreak.

There would be great differences in the cost of paying for health care, and who is liable for payment.

There would be no compensation to farmers who were misidentified as growing an outbreak crop. There would be no exemption from liability for the farm that caused the outbreak, because they have strict liability for putting out adulterated food.

There would be no presumption that “organic is safer.”  There are still major constituencies for whom organic production is an ambiguous, minor but often irritating fact of life in farm and food production industries. They could condemn an outbreak as due to being organic (8), rather than despite being organic, as in the EU.

A final question from the O104:H4 outbreak: what can be done to improve the safety of raw sprouts, whether produced on an organic farm or a conventional farm?

For the actual production process itself there were only two factors: seeds and water. Sprouts were produced with clean equipment in a well-sanitized manner. There is a minimal ecology to sprout production, which may be part of the problem.

Changing from sprouts to greenhouse production of baby vegetables in soil might seem to be a minor change, (let the sprouts grow some true leaves!), but the research on both greenhouse and field production indicates that human pathogen uptake from the soil to plants is highly inhibited, and this can include seed-borne human pathogens.

In a practical sense, sprout safety requires either human pathogen-free seeds specifically produced for sprouting, a kill step that can be used after seeds are sprouted and pathogens are exposed for treatment, or both. People could also cook their sprouts, the original use for soy sprouts from the very beginning of soy as a major food in China (9).

The rational basis for organics includes an ecological approach to farming and an ap- preciation for the biological opportunities and constraints on and around their farms. Conventional farmers can use the same approaches and often do.

I also see sprout production, and the history of sprout outbreaks in this country, as a metaphor for the current approaches to regulating food safety on farm. There could not be a more simplified system for contained and controlled food production than sprouts,

yet it fails repeatedly. Applying the same approaches used in sprout production to the complexity of farms and the farm environment seems both irrational and doomed to fail.

1) Epidemic Profile of Shiga-Toxin-Producing Escherichia coli O104:H4 Outbreak in Germany N Engl J Med 2011; 365:1771-1780 November 10, 2011


(2) STEC Workshop Reporting Group. Experiences from the Shiga toxin-producing Escherichia coli O104:H4 outbreak in Germany and research needs in the field, Berlin, 28-29 November 2011 . Euro Surveill. 2012;17(7):pii=20091. Available online:


Date of submission: 10 February 2012

(3) Eurosurveillance, Volume 17, Issue 4, 26 January 2012 Rapid communications OUTBREAK OF HAEMOLYTIC URAEMIC SYNDROME DUE TO SHIGA TOXIN-PRODUCING ESCHERICHIA COLI O104:H4 AMONG FRENCH TOURISTS RETURNING FROM TURKEY, SEPTEMBER 2011 N Jourdan-da Silva1, M Watrin2, F X Weill3, L A King1, M Gouali3, A Mailles1, D van Cauteren1, M Bataille4, S Guettier4, C Castrale5, P Henry5, P Mariani6, V Vaillant1, H de Valk1




 (5) Appl Environ Microbiol. 2012 Feb;78(4):1302-7. Epub 2011 Dec 16.

Validating Thermal Inactivation of Salmonella spp. in Fresh and Aged Chicken Litter.

Kim J, Diao J, Shepherd MW Jr, Singh R, Heringa SD, Gong C, Jiang X. http://aem.asm.org/content/early/2011/12/12/AEM.06671-11.short?rss=1

(6) The greatest contribution to food safety in the future might be to require biology and microbiology courses for economics students. And there is an interesting possibility that the ethical considerations used in designing organic rules for animals will be shown to also have had long term economic value.

(7) For example, I happened to be at one of the organizing meetings for the CA LGMA when CFSAN investigators revealed that the farm associated with the spinach outbreak was organic in transition. The chief scientist of a major produce organization exclaimed “We were so close!” Perhaps he was under stress. The same attitude came from state senators at a California hearing on the same crisis. “Suppose I don’t want my food grown organic with manures.” Most outbreaks and recalls are in conventional produce and it looks to me like there are fewer outbreaks due to organics than a proportional expectation would predict.

(8) GMO biotechnology companies sometimes have an ambiguous relationship to organic food production. When they want to avoid labeling GMO crops and foods they can point consumers to organics, where GMO is prohibited. When organic farmers block release of crops like GMO herbicide-resistant alfalfa, they get incensed. The USDA’s official position for the last few years has been “people; we can all get along.”

(9) See page 296 of H.T. Huang’s magisterial Fermentations and Food Science; Volume VI: 5 of the series Science and Civilization in China (Joseph Needham). Cambridge University Press, 2000. The first written documentation of soy sprouts in Chinese history includes the steps: wash after three days and fry in oil.


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Sizing Food Safety Regulations to Fit the Farm https://www.storkxx.com/2012/02/farming-on-the-brink-a-perspective-on-2011/ https://www.storkxx.com/2012/02/farming-on-the-brink-a-perspective-on-2011/#respond Thu, 16 Feb 2012 09:59:07 +0000 http://foodsafetynews.default.wp.marler.lexblog.com/2012/02/16/farming_on_the_brink_a_perspective_on_2011/ Continue Reading]]> Food safety issues and worries about food safety rose to a high level last year among farmers. The owner of one of the original small organic farms in my county asked me what lessons could be learned from the E. coli O104:H4 outbreak in Europe, but then came E. coli O157:H7 on strawberries in Oregon, Listeria on cantaloupes in Colorado and the FDA rulemaking process for farm food safety.

What exactly is a small farm?

The last Census of Agriculture data is from 2007, although a new census will be made this year. In 2007, there were 2.2 million “farms.” About 1.3 million of these had farmgate gross sales of less than $10,000. Only 57,000 of them had farmgate sales of $1 million or more (sales, not profit). (1)

This is about the sales volume of a medium-large urban food co-op in the 1970s, 40 years ago, when a million was worth a million, you might say. All of agriculture in the U.S. had farm sales of around $300 billion, roughly equivalent to a single major multi-national oil company.

Almost all the farmers I work with are part of the 57,000. But the 57,000 are as stratified as the whole farm population. About 10 percent of them (5,600) have farmgate gross sales of $5 million or more. Some of the farms I work with are among those 5,600. The USDA doesn’t break down the 5,600 any further, but there are also a wide range of farm sizes within the category “$5 million or more.”

Some are truly ‘superfarms’ with significant share of production of an entire commodity. When I analyzed California leafy greens using the 2002 Census of Agriculture data, for example, 59 lettuce farms grew 69 percent of the state lettuce crop on 1,000 acres or more. In 2006, USA Today reported that a single spinach grower produced almost all of the spinach for Fresh Express, at that time the largest fresh-cut processor in the country.

What is the definition of a “superfarm”? There are both organic and conventional vegetable operations in California that farm more than 20,000 acres — almost 30 square miles. They could certainly qualify, but where the cutoff would be is not clear. Some are simply outstanding operations, including for food safety. Perhaps 10 percent of the farms with sales above $5 million, or about 500 farms, have very large roles in many produce categories.

In 2011, the USDA’s Economic Research Service published “Financial Characteristics of Vegetable and Melon Farms” by Mir Ali and Gary Lucier, which shows continuing concentration across all vegetable and melon types (2).

The fact that the same individuals may control more than one farm “entity” complicates matters, but in general this means that farm statistics understate the degree of concentration and disparity between farm sizes.

The term “farms” includes farms and ranches, both crops and animal production, including large CAFOs (concentrated animal feeding operations), as well as woodland and pasture farms.

It’s pretty easy to guess that the 1.3 million farms with less than $10,000 in sales should be in the “very small” farm category. But where this category ends is not clear.

The Tester Amendment to the Food Safety Modernization Act, under which the FDA is writing new farm food safety regulations, establishes a kind of definition of small as less than $500,000 in (farmgate) sales and selling most production “locally” within a state, or within 275 miles if sales cross state lines. From my perspective, and looking at the O104:H4 outbreak in Germany, this sounds more regional than local, but regional is not a defined category.

The FDA briefly describes the FSMA as follows:

“FSMA is the most sweeping reform of FDA’s food safety authority in more than 70 years, and a law of this scope and complexity often comes with direction from Congress for the federal agency responsible for implementing it to go through a process called rulemaking…”

Under the new food safety law, FDA will be issuing a number of rules including a preventive controls rule in food facilities, a foreign supplier verification rule, and a produce safety rule.”

For farmers, the question of how a “food facility” is defined — because it can include on-farm basic operations — and how rules for produce are developed, and where federal regulation stops and state regulation takes over, are all crucial questions, which are partly dependent on the size of the farm being “small” or not. Very different language is used by different parts of the industry for both “small” and “local.”

One could say that a small farm has average annual sales somewhere in the range of from $10,000 to about $500,000, but less than $1 million dollars, recognizing that a lot of jockeying is going on because of the legal implications of the categories for food safety. By this very inclusive definition, there are about 840,000 “small farms,” if by “small” you include what might be more reasonably called “medium” or “medium-large” farms.

There are no “average” farms except as an inappropriate statistical fiction.

Crops are not evenly distributed geographically. For example, California grows about 1/2 of U.S.-produced fruits, vegetables and nut crops, and for produce like leafy greens, the Salinas valley and the desert production of the Imperial Valley and Arizona dominate U.S. production in very specialized sub-regions, which are often dominated in turn by the largest farms. 

It might make more sense to write leafy green regulations geared toward the largest farms in these areas rather than trying to impose a one-size-fits-all on smaller farmers growing a variety of crops in varying climates and geography. Many fruits and vegetables to be regulated as “produce” have similar concentrations, with large farms producing much of the crop in specific regions.

Just using very broad statistical indicators, it should be obvious that U.S. agriculture is highly heterogeneous. At an ecological, geographical, geological, biological, social, and farm or farm-field level the heterogeneity is infinitely more complex.

It does not seem like a rationally conceivable project to write national regulations for food safety on-farm, although it may be legally mandated.

Not, that is, if by regulation one means detailed instructions for every farm and farm size and crop and diversity of production and integration of production between crops and animals and ecosystem interactions and farm benefits to the environment. Even looking just at what I look at (mostly) in food safety, the production of “specialty crops” (fresh vegetables, fruits, nuts and other raw products), U.S. farm complexity defeats centralized rule-making that could function.

The knowledge needed, if anywhere, is in the fields.

One could get far more impact for every regulatory buck spent if the initial goal were the regulation of the 6,000 largest farm operations. These truly approach what we think of as “industrial agriculture,” with very large field sizes — often in large monocultures, and often collectively dominating the overall production of a particular commodity.

They have many characteristics in common and look like the place one could start implementing national regulations. One could make sure these 6,000 farms had good food safety procedures and then perhaps move on to the next 50,000 farms with sales over $1 million — a tougher nut to crack but conceivable. If we had well-validated food safety procedures f
or the very largest farms, that is. Do we?

Apparently not. Otherwise hundreds of millions of dollars of ongoing and new research projects — federal, state, and private — would not be going into fundamental and operational (or validational) research on farm food safety, in particular aimed at these kinds of farms. A several-year study headed by the University of Maryland will for the first time

have some access to the private data of the largest produce farms and processors, for example.

There is a further problem in fitting on-farm food safety to the scale of farming. If one looks at some of the metrics and “‘supermetrics” developed by groups like the California Leafy Green Marketing Board and private buyers, respectively, it looks to me like the very largest farms and superfarms have the best fit to the metrics and face the least economic damage from applying them.

One of the metrics commonly used is to buffer production away from natural habitat. This can be a reasonable issue for a 1,000 acre field situated on a multi-thousand acre production farm. But it gets more expensive the smaller the field and the closer the natural habitat. At the limit of difficulty would be a small field, close to habitat, where the requirements for buffering (set on a national standard) leave no field left to farm.

But my impression is that economic constraints start with even quite large farms.

There is quite a lot of well-validated data, not on how to farm safely, but on how to farm unsafely in particular ways, on how to specifically screw up. Some of these are general principles that appear truly scale neutral. Some are commodity-specific and one hopes reflected in parts of the commodity-specific guidances by the FDA and others, and are mostly scale neutral.

The human pathogens of major concern in food safety have their individual ecologies and preferences. Situations where each pathogen thrives can be looked for. These include Shiga toxin-producing E. coli (such as O157:H7), Listeria, Salmonella, Shigella and Campylobacter. There are also common pairings between a particular crop and a particular pathogen found to be of greatest concern for that crop. Salmonella on cantaloupes is a common pairing.

So I could imagine several thousand pages of regulations being written for food safety on “small” and “very small” farms being replaced, instead, by one sentence: “Don’t screw up.” 

For example: “Don’t harvest strawberries, produced near ground level, next to wild animal droppings. And if rain or sprinkler irrigation could have splash-dispersed potential pathogens, expand the area where there is no harvest.”

This is a strategy of known defect reduction, or elimination, often used in sensory control of food quality. Defect reduction is an achievable process of improvement on any farm. It would seem to be more effectively approached through education and cooperative efforts, leaving farmers in control — as they should be. They know their farms. It could have dramatic impact, over time, in reducing food safety hazards on-farm. This is a statistical reduction of harm, effective on average, and not a guarantee. There are fairly simple steps that farmers have control over that would increase food safety.

On the farm, water quality, presence of excrement that can contact a crop, worker health, and crop “handling” — preparation for sale off farm — seem to be the main hazard points under control. Yet most regulations try and comprehensively detail every aspect of growing a crop. Growing crops up until harvest might be the least important factor in increasing overall food safety. The steps from harvest to the consumer are the places that seem to have the greatest impact on food safety. Those steps include handling, processing, commingling, storing, packaging, labeling (such as use-by dates, use-instructions), transportation (and consumer or retail behavior), which can have far more destructive effects. Except insofar as a grower is involved in all of these, they remain out of the grower’s control.

In 2007, we found that processor/handlers of whole produce, and fresh-cut products, were the known sources of many multistate produce outbreaks and recalls over the previous 20 years.  We also found that fresh-cut produce, compared to whole produce, looked like the cause of more outbreaks than would be the case if on-farm contamination was all that mattered.

For E. coli O157:H7 and many produce categories like leafy greens, we came up with the notion that the introduction of a new pathogen into a new kind of processing and food category without a kill step — fresh-cut for both retail and food-service/wholesale — combined with certain commercial realities to create the majority of the outbreaks and recalls in the U.S. (3). Consequently, the greatest impact on food safety would come from better and specific regulation of the fresh-cut industry, or self-regulation for that matter, rather than regulating “farms.”

One type of regulation that, from the record, could have great impact is simply to have use-by dates on bagged fresh-cut produce for consumers, or containerized fresh-cut for food service, be determined with food safety criteria, as well as by “freshness” and, in fact, to be under some regulation of any kind.

The three outbreaks in 2011 mentioned at the beginning of this commentary show the limitations of this approach as the sole analysis — it is only true as far as it goes.

(1) 2011 Census of Agriculture

 (2) Financial Characteristics of Vegetable and Melon Farms 

(3) September 22, 2009 testimony of David Runsten, Director of Policy and Programs, Community Alliance with Family Farmers, Davis, California, at the USDA hearing on the proposed National Leafy Green Marketing Agreement, Monterey, California


Daniel B. Cohen is the owner of Maccabee Seed Co., an agricultural research-and-development and consulting company in Davis, CA.

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A Parallel Clinical Pattern to O104:H4 https://www.storkxx.com/2011/07/a-parallel-clinical-pattern-to-o104h4/ https://www.storkxx.com/2011/07/a-parallel-clinical-pattern-to-o104h4/#respond Wed, 06 Jul 2011 01:59:04 +0000 http://foodsafetynews.default.wp.marler.lexblog.com/2011/07/06/a_parallel_clinical_pattern_to_o104h4/ Continue Reading]]> The O104:H4 serotype has an unusual clinical pattern for Shiga toxin-producing E. coli (STEC) pathogens, including bloody diarrhea in adults followed by a high conversion rate to adult hemolytic uremic syndrome (HUS) or to severe non-HUS enterohemorrhagic symptoms in adults.

There is another STEC group that parallels the unusual pattern of the current outbreak in Germany. It as characterized by a form of Shiga toxin that becomes more deadly after it is attacked by the patient’s body’s defense mechanisms.

Most STEC like O147:H7 have a class of Shiga toxin known as Stx2. But there are a variety of subtypes of Stx2 such as Stx2a, Stx2b, Stx2c Stx 2d and others. There is a form of Shiga toxin Stx2d that becomes more virulent following attack by the mucosal enzyme elastase, whether from mice or humans.

Elastase attacks the toxin by cleaving off two amino acids from one of its components, at the C-terminal end of the A2 peptide (short protein) of Stx 2d. In lab tests with mouse models in 2002, as well as other tests, conducted by Dr. Alison O’Brien’s group at the Uniformed Services University of the Health Sciences (Bethesda, Maryland), these E. coli with toxins activated by exposure to mucosal preparations or the specific enzyme elastase, were more virulent than any other (STEC) Stx E.coli strains [1].

This type of Shiga toxin was then named “Stx 2d activatable” because instead of damaging the toxin by splitting it, the elastase, or crude mucosal preparation containing elastase, made it worse — “activating” it.

Professor Dr. Helge Karch and associated researchers at the National Consulting Laboratory on Hemolytic Uremic Syndrome, University of Muenster and the Interdisciplinary Center for Clinical Research, Muenster, wanted to study what the clinical implications of this kind of strain were for humans, rather than mice. They did a stratified analysis of 922 human STEC strains from patients with HUS, bloody or nonbloody diarrhea and asymptomatic carriers, looking at different kinds of STEC strains and disease course outcomes.

It takes more than Shiga toxin to have a virulent STEC pathogen. In particular, in “normal” STEC strains, tissue invasion is aided by an adhesive protein called intimin, encoded by the eae gene. In most STEC descriptions, having the eae gene for intimin is a crucial component for pathogenicity.

The Muenster researchers found that Stx2d activatable strains were also highly virulent in human cases, not just in mice or the in vitro model of Vero cells (the basis of calling Shiga toxins “verotoxins” is based on this kind of test). This was despite being eae (-), lacking the production of intimin. They also found the unusual pattern of adults and older patients with bloody diarrhea and HUS, as in the O104:H4 outbreak [2,3].

There were several alternative hypotheses to explain this. One was that the increased virulence of the activated toxin was a compensation for lack of intimin, or that toxin delivery into tissue was actually aided by the peptide editing caused by human mucosal elastase. A second possibility was that there was overexpression of the Stx gene to compensate for lack of intimin. A third possibility was that Stx2d activatable STEC strains had an unknown virulence factor that replaced the intimin functionality.

The first characterization by the Robert Koch Institute of the German O104:H4 outbreak strain included the notation that it was also eae (-), lacking intimin. Rather like the third hypothesis for Stx2d activatable strains, the outbreak strain had different adhesion genes characteristic of the entero-aggregative types of pathogenic E. coli, not seen in a “normal” STEC outbreak, whether in O157:H7 or pathogenic non-O157s.

Here the close parallel ends.

The O104:H4 outbreak strain, has no need for intimin, one might say, since it has other adhesion and invasion factors from its enteroaggregative genetic background. O104:H4 appears to be an enteroaggregative type of E. coli with Shiga toxin functionality from normal STEC. It is in a sense, a Shiga toxin containing enteroaggregative strain type. It could be

described as a STEC “armed” enteroaggregative E. coli or as a hybrid of STEC and enteraggregative types.

Virulence and adult bloody diarrhea and adult HUS at a higher rate of conversion may be due entirely to these enteroaggregative derived genes, not due to increased virulence of the Shiga toxin subtype, or increased virulence due to peptide editing by elastase, or some other enzyme.

The DNA sequence of the toxin from O104:H4 is supposed to be the same as Stx2, not Stx2d-activatable.

However, the 5-day time course from bloody diarrhea to HUS is somewhat suggestive of a pathogen-human-pathogen interaction like that of mucosal elastase and Stx2d activatable strains. Indicators of patient status slightly improve on the third day, and some patients think they are recovering just before plunging into a rapid development of HUS.

It is possible that this reflects a similar trigger, where toxin is functionally enabled for increased virulence and rapidly deployed in response to the same human defenses that give patients or physicians the illusion of pos- sible improvement.

STEC strains can change and evolve even during the infection course of a single patient (3), losing or gaining plasmids and phages, with their associated functionalities for Shiga toxin or intimin or drug resistance, for example. The parallel unusual clinical patterns between the O104:H4 outbreak strain and STEC Stx2d activatable pathogenic strains — severity of adult clinical symptoms — may be an example of convergent evolution, getting to the same results by completely different mechanisms. The mechanism could also be analogous or very similar, if not identical.

Regardless of mechanism, two parallel types of cases, with similar clinical pattern and outcomes, can still give clinicians and researchers sugges- tions for approaches, context and comparisons for treating the disease course.

Daniel B. Cohen

Maccabee Seed Company

Davis, CA

[1] Martina Bielaszewska, Alexander W. Friedrich, Thomas Aldick, Robin Schürk-Bulgrin, and Helge Karch Shiga Toxin Activatable by Intestinal Mucus in Escherichia coli Isolated from Hu- mans: Predictor for a Severe Clinical Outcome Clin Infect Dis. (2006) 43(9): 1160-1167 doi:10.1086/508195

[2] “A subset of eae-negative STEC strains (i.e., STEC that produce Stx2dactivatable) differ from other eae-negative STEC strains by their strong association with severe disease… By its association with severe outcome of the infection caused by eae-negative STEC, Stx2dactivatable parallels the pathogenetic significance of Stx2 among eae-positive STEC … However, in contrast to Stx2, which is associated with HUS development in children <5 years old…, most of the patients with HUS from whom we isolated Stx2dactivatable-producing STEC were adults.” From Bielaszewska et al., next citation.

[3] Activation of Shiga toxin type 2d (Stx2d) by elastase involves cleavage of the C-terminal two amino acids of the A2 peptide in the context of the appropriate B pentamer. Melton-Celsa AR, Kokai-Kun JF, O’Brien AD Mol Microbiol. 2002 Jan;43(1):207-15.

[4] Alexander W. Friedrich, Wenlan Zhang, Martina Bielaszewska, Alexander Mellmann, Robin Köck, Angelika Fruth, Helmut Tschäpe, and Helge Karch  Prevalence, Virulence Profiles, and Clinical Significance of Shiga Toxin-Negative Variants of Enterohemorrhagic Escherichia coli O157 Infection in Humans. Clin Infect Dis. (2007) 45(1): 39-45 doi:10.1086/518573

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Notes, Observations on Europe's Epidemic https://www.storkxx.com/2011/07/clinical-epidemiological-notes-from-the-outbreak/ https://www.storkxx.com/2011/07/clinical-epidemiological-notes-from-the-outbreak/#comments Tue, 05 Jul 2011 01:59:02 +0000 http://foodsafetynews.default.wp.marler.lexblog.com/2011/07/05/clinical_epidemiological_notes_from_the_outbreak/ Continue Reading]]> What are the lessons learned so far from the O104:H4 outbreak?

German medical and public health authorities are burdened by the equivalent of more than 10 normal years worth of case loads occurring in a single month, the continuing need for secondary infection prevention, the outbreak source investigation and perhaps other issues as well. Despite this, a major study conducted as the outbreak was peaking was published in the New England Journal of Medicine [1]. This included a prospective study on a subset of patients.

An article [2] and editorial [3] published in Eurosurveillance also presented some key information. The specific content of these reports and their implications for medical and public health response to possible new clusters or outbreaks remains largely unreported, two weeks later. Here are some of the vignettes and possible lessons learned based on these three reports, news articles during the development of the outbreak — largely from Germany — reports from the French outbreak, and other background sources.


One of the important findings of the prospective study in the NEJM article [1] was that daily laboratory testing for platelet counts, creatinine and lactase dehydrogenase (LDH) were crucial for monitoring the approach of HUS in patients.

It took a median of 5 days, from known (bloody) diarrhea to HUS onset, when this occurred. For the first three days levels were fairly steady, and in fact platelet counts and LDH, if anything, improved. This corresponded with some patients re-porting that they felt they had begun to recover from bloody diarrhea even as HUS was about to rapidly develop.

On day four creatine and lactate dehydrogenase rose modestly, while platelet levels began a somewhat steeper corresponding decline. During day five creatinine levels had tripled over the baseline; lactase dehydrogenase had tripled or quintupled and platelet levels had fallen to about one fifth of baseline (50-60,000 platelets per cubic mm from the chart).

These were the accurate predictors for HUS; indicating kidney damage response (creatinine), tissue damage response (lactase dehydrogenase) and the consequence of blood cell damage (platelet decrease) or hemolysis.


The Eurosurveillance article [2] presented one of the first highly probable human-to-human transmissions in this outbreak, in this case mother to infant.

Returning from northern Germany to the Netherlands, the mother became ill 8 days later, and the child 15 days later. The mother developed severe HUS 4 days after admission to the hospital for bloody diarrhea. Her child developed “blood abnormalities compatible with HUS,” fever — which appears unusual for these cases — and severe neurological symptoms. Three weeks after admission, as of the reporting date, the child remained on dialysis and had unknown neurological consequences.

This fits with a reported pattern of approximately 8 days for incubation of O104:H4 [1], about twice as long as for O157:H7. The timing of HUS onset also fits with the NEJM description of timing of HUS approximately 5 days after initial admitting symptoms — here bloody diarrhea and abdominal pain for two days for the mother.

Crucially: “The child had spent much time with her mother during her stay at the first hospital, when the mother developed diarrhea. Before admission of the child to (the hospital) the mother had not been advised to take any specific hygienic measures.”


One of the most important findings reported in the Eurosurveillance editorial [3] was that roughly one half of patients with HUS developed severe neurological symptoms. These included: disorientation, dissociation, stupor, and life-threatening seizures. Neurological symptoms, present in other Shiga toxin-producing E. coli (STEC) outbreaks, are a signature severe partner to HUS and gastroenteritis in outbreaks with this strain of O104:H4 (See also [7]).


Clinical presentations from this outbreak are quite surprising compared to past experience both with O157:H7 and non-O157 STEC E. coli cases over the last 30 years.

Some of this can be explained, perhaps, by the presumed food carrier being sprouts. Most cases are adults, who may be presumed to be more likely to eat sprouts than those 17 years or younger. More cases are adult women, in particular, than would be expected at random. This also could be explained by dietary choice. The vast majority of deaths are in older and elderly patients. This could be explained by the observation that there still are no effective treatments for HUS in particular, and that the elderly may be less successfully treated by ameliorative or palliative care, or may in fact be more susceptible to harm from some of the treatments.

However, in comparing adults and children, the O104:H4 outbreak is not only different from expectations but backward from previous experience. In the past, HUS has been a disease outcome overwhelmingly of infants and children, but here it is overwhelmingly an adult outcome. Bloody diarrhea is more common in adults while vomiting is more common in children.

The disease course, once started by dietary or human-to-human transmission, is statistically very different for adults and children compared to other STEC.


Another, much smaller O104:H4 outbreak occurred in the Gironde region of southwest France centered on Begles [4]. This outbreak has 15 cases versus more than 4,000 in the German outbreak. The outbreak strain is consistent with the May-June outbreak strain in Germany.

“Preliminary data indicate that this outbreak shares the same novel epidemiological, clinical and microbiological features identified in the E. coli O104:H4 outbreak in Germany [8], including a predominance of adult women among the cases, an unusually high proportion of HUS cases among identified possible outbreak cases, a longer median incubation period than expected for cases of Shiga toxin-producing E. coli infection, and a genetically related E. coli O104:H4 producing a CTX-M ESBL.”

In this case three kinds of sprouts were produced for a local event. The first food surveys came back with little in common, but further epidemiological questioning showed the initial patients had in fact consumed cold foods decorated with the sprouts at the same event.

Because there is an overlap of a seed supplier with the German sprout producer/farm, fenugreek seeds purchased from Egypt from two different years’ stocks are leading candidates for possible seed-borne transmission through sprouts.

Because of the mult
possibilities of routes of contamination, however, European health authorities are being much more reserved in their comments than earlier. The UK seed company involved in distribution questioned how seeds sold for sprouts to many locations could cause an outbreak in only one location if they were, in fact, the source.

The French case also illustrates a problem raised by U.S. epidemiologists: how to distinguish different reporting criteria when describing the outbreaks. Using the French data, it would look like a 50% transition rate from bloody diarrhea to HUS vs a 20% rate in Germany.


Medical treatment and follow-up need to be planned before patients see a doctor or are admitted to a hospital until after patients are no longer contagious, if that can be determined.

The mother to child transmission case from the Netherlands shows the terrible individual consequences of the failure to have a system in place for comprehensive care, including family care. In a mass patient event, pre-planning may be critical to limit secondary transmission.

Patients reported in the German press going to doctors or hospitals with preliminary symptoms including diarrhea and stomach cramps, but basically being discharged to return home without treatment or follow-up and told to come back if they developed bloody diarrhea. When this did develop and they returned, they found that while there was segregation of potential STEC patients, the conditions were horrendous, including one bathroom for more 100 patients. Sanitation efforts were quickly overwhelmed. One patient commented that if she wasn’t sick before, she would be now.

German press reports also showed there was great concern and confusion among families of patients about how to treat their family members who were returning home from the hospital. There was apparently a lack of follow up or information provided.

There may need to be special training for both conventional medical staff, social workers or other paraprofessionals to provide accurate care before admission, at admission, and to provide follow-up care and information after returning home in a mass event.


German press reports showed pro-active actions by public health authorities to prevent child to child transmission in school settings. This included segregating or keeping home children who were ill, shutting down and sanitizing classrooms, and in one case where both food worker employees and children became ill, closing an entire school. It is not clear where children who may have been ex- posed to carriers actually went.

The presumption from O157:H7 experience is that children would be slower to clear STEC from their system than adults, taking a median time of something like 30 days. There also is a reasonable presumption that children may have more difficulty understanding and carrying out basic sanitation, either because of im- maturity or lack of adequate facilities.

O104:H4 may act differently in this regards as well, however. It infects children and adults differently than in O157:H7. If it acts more like some enteroaggrega- tive strains, then adult food handlers may be more of a concern (5), although the complexity of this group makes any generalization difficult (6).

The reports of probable person to person transmission from visitors to Germany to other countries include at least one case in the United States, and possibly two, where the second case was fatal. The impression is that most of these cases, relatively few so far, were adult to adult. Adult transmission should be considered in food handling, indirect hand to mouth transmission through different media such as some cosmetics, or intimate contact, including sex. But there has been little discussion of any of these potential routes.

There have been no reports of multiple transmissions from passengers returning from Germany by air, despite closed, shared facilities.



Most of the lessons on acute care of O104:H4 won’t be known until the German public health and medical personnel have the time to collate, evaluate and un-derstand their experiences.

There were reports that some physicians and hospitals were trying aggressive early treatment with antibiotics. Normally this is not recommended because of the potential for releasing even more Shiga toxin, but the press reports were that they found normal procedures were not working. These would presumably be antibiotics that O104:H4 does not have resistance markers to. The employment, timing, follow-up, efficacy and consequences for further resistance selection to new classes of antibiotics all have to be a concern.


In previous STEC outbreaks patients with central nervous system (CNS) dys- function as well as HUS had worse outcomes and mortality. In a 2010 review F. Obata suggested the evidence points to a weakening of both the blood-brain barrier and the blood-cerebrospinal barrier, possibly with the direct involvement of Shiga toxin Stx-2 subtypes involved [8].


One of the features of clinical treatment in the O104:H4 outbreak has been greater deployment of monoclonal antibodies (MAb’s) targeted at different com- ponents or actions of Stx.

One private company made their MAb drug freely available. This was targeted at disrupting one of two mechanisms of hemolysis, the disruptive triggering of apo- posis, normally a genetically controlled coordinated induction of cell death (9). A second method of triggering hemolysis involving Stx is the disruption of ribo- somal structures in cells preventing protein synthesis and causing cell death [10].

Alison D. O’Brien (10) and her lab at the Uniformed Services University of the Health Sciences in Bethesda MD has conducted some of the key research on monoclonal antibodies to target shiga toxin function and STEC pathogenicity for many years. Some of the commercial products came from earlier research at this lab. A number of animal models have been used by different labs with results that seem consistent with clinical experience (see [11]).

The overall efficacy of MAb’s and passive antibody therapy in the outbreak will be worth learning. There was one point made in the Eurosurveillance editorial [2]:

“Worryingly, especially patients with seizures seemed to respond only weakly to standard antibody-based treatment regimes.”


There could be a role for vaccination against STEC E. coli, particularly for limited use to prevent li
kely secondary infections alongside other methods [12].

For O157:H7 there are two commercial vaccines developed for cattle. These were tested in herds in both Canada and the United States to see if they would cause a reduction in O157:H7 numbers and shedding, helping protect beef against being a carrier. Apparently they are not being commercially used.

This is a similar situation to West Nile Virus vaccines, where at least three commercial vaccines are available and in use for horses, but none for humans. Vaccine development to prevent STEC infections in people may require a different business or nonprofit model.

Reports on household members of primary cases who remained healthy have shown different levels of antibodies to Stx and to O157:H7 in both IgG and IgM classes. If an IgM was effective at all, oral vaccination might be effective and a more acceptable means of prevention of spread including mass inoculation.


Author’s note.

I am quite aware of my limitations in preparing this kind of review, but I also note that communication between medical subspecialists and the general public are difficult. Sometimes the general public includes other medical professionals in differing specialties who may be impacted by a new outbreak of O104:H4 yet not have followed the literature from Europe on this issue.

To reflect my lack of expertise, I borrowed the presentation format of the late columnist Herb Caen (San Francisco Chronicle for most of his long career). This was known as “three dot journalism” where he mixed gossip, reporting, social commentary, culture, politics, tragedy and profundity into a city-wide swirl. I suppose one could call this “three dot medical journalism.”

Food Safety Website has space for comments, and in this case I would especially invite medical and epidemiological comments to correct errors of content or interpretation or new information.

Daniel B. Cohen

Maccabee Seed Company

Davis. CA


[1] Epidemic Profile of Shiga-Toxin-Producing Escherichia coli O104:H4 Outbreak in Germany — Preliminary Report

Christina Frank, Ph.D., Dirk Werber, D.V.M., Jakob P. Cramer, M.D., Mona Askar, M.D., Mirko Faber, M.D., Matthias an der Heiden, Ph.D., Helen Bernard, M.D., Angelika Fruth, Ph.D., Rita Prager, Ph.D., Anke Spode, M.D., Maria Wadl, D.V.M., Alexander Zoufaly, M.D., Sabine Jordan, M.D., Klaus Stark, M.D., Ph.D., and Gérard Krause, M.D., Ph.D. for the HUS Investigation Team

June 22, 2011 (10.1056/NEJMoa1106483)

[2] Kuijper EJ, Soonawala D, Vermont C, van Dissel JT. Household transmission of haemolytic uraemic syndrome associated with Escherichia coli O104:H4 in the

Netherlands, May 2011. Euro Surveill. 2011;16(25):pii=19897. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19897

(3) Jansen A, Kielstein JT. The new face of enterohaemorrhagic Escherichia coli infections. Euro Surveill. 2011;16(25):pii=19898. Available online:


[4] Gault G, Weill FX, Mariani-Kurkdjian , Jourdan-da Silva N, King L, Aldabe B, Charron M, Ong N, Castor C, Macé M, Bingen E, Noël H, Vaillant V, Bone A, Vendrely B, Delmas Y, Combe C, Bercion R, d’Andigné E, Desjardin M, de Valk H, Rolland P. Outbreak of haemolytic uraemic syndrome and bloody diarrhoea due to Escherichia coli O104:H4, south-west France, June 2011. Euro Surveill. 2011;16(26):pii=19905. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19905

[5] Oundo, J. O., Kariuki, S. M., Boga, H. I., Muli, F. W. and Iijima, Y. (2008), High Incidence of Enteroaggregative Escherichia coli Among Food Handlers in Three Areas of Kenya: A Possible Transmission Route of Travelers’ Diarrhea. Journal of Travel Medicine, 15: 31-38. doi: 10.1111/j.1708-8305.2007.00174.x

[6] Q&A: Dr. Robert Tauxe on the Outbreak in Germany, by Daniel B. Cohen, June 22, 2011, Food Safety Website.

[7] “Doctors Shaken By Outbreak’s Neurological Devastation; At first, doctors were most concerned about the kidneys of patients with enterohaemorrhagic E. coli, or EHEC. In the past week, howver, it has become apparent that neurologi- cal side effects of the bacterial infection could be even worse”. By SPIEGEL Staff. Spiegel Online 06/09/2011.

[8] Adv Appl Microbiol. 2010;71:1-19. Epub 2010 Feb 20. Influence of Escherichia coli shiga toxin on the mammalian central nervous sys-

tem. Obata F

(9) Induction of apoptosis by Shiga toxins. Vernon L Tesh. Future Microbiol. Author manuscript; available in PMC 2011 January 1.Published in final edited form as:Future Microbiol. 2010 March; 5: 431-453. doi: 10.2217/fmb.10.4.

[10] Mouse Models of Escherichia coli O157:H7 Infection and Shiga Toxin Injec- tion. Krystle L. Mohawk and Alison D. O’Brien. J Biomed Biotechnol. 2011; 2011: 258185. Published online 2011 January 3. doi: 10.1155/2011/258185.

[11] Stx2- but not Stx1-specific human monoclonal antibody protects piglets chal- lenged with enterohemorrhagic Escherichia coli producing Stx1 and Stx2. Kwang-il Jeong, Saul Tzipori, and Abhineet S. Sheoran. Published in final edited form as: J Infect Dis. 2010 April 1; 201(7): 1081-1083. doi:10.1086/651198

[12] Strategies to Reduce Person-to-Person Transmission during Widespread Escherichia coli O157:H7 Outbreak. Edmund Y.W. Seto,* Jeffrey A. Soller,† and John M. Colford Jr. Emerging Infectious Diseases, Vol 13, No. 6, June 2007.

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