When AP reported this week that an owner of Jensen Farms was being fined by the U.S. Department of Labor for failing to provide safe migrant worker housing, I must admit even I was a bit shocked. Could it be that an owner of a business that allowed the deadly fecal bacteria Listeria to coat
America’s 50 Most Powerful People in Food for 2012
#46. Bill Marler, Foodborne Illness Lawyer and Attorney – So says the Daily Meal.
In the last several days since my father died, I have been putting things in the context of what he would think or say. “As one friend put it, once your parents are gone, you are ‘on deck.’ Another the
LAWRENCE EMMETT MARLER JR. – 1929 – 2012
My father died last evening. I had the honor of being with him for the last days, hours, minutes and seconds of his long life. A former high school and college basketball star, Korean War veteran, college math teacher, gentleman farmer and fisherman – but never a “former” marine, my dad died on his own
Hey, email me your mailing address after you subscribe
A few days ago I posted this:
A few months ago I offered to give a book to each new person who subscribed to my blog up to 500 – I have 200 hardcover books left (now about 50). So, the next 200 new subscribers will get a free hardcover book.
I then added:
Where the Hell did Shiga Toxin E. coli come from? A Literature Review – Part 1
In recent months, a surge of papers have appeared in the literature describing findings from the deadly 2011 E. coli O104:H4 outbreak in Germany linked to sprouts (2-10, 12-14). The speed at which this information is being published in the literature—much of it free to the public through open access journals—is a testament to the advances in biotechnology available to scientists that study emerging foodborne pathogens. However, despite all the impressive molecular tools the researchers’ have at their disposal, the origin of the unusual strain associated with the outbreak in Germany is still unknown. In fact, the origin of E. coli O157:H7, a bacterium first described in the 1970s and currently the most well studied shiga toxin-producing E. coli (STEC) strain, also (despite conventional wisdom) remains elusive.
Introduction
So, I ask, where the hell did E. coli O157 and other STECs come from?
If you read the media stories and foodist blogs, it would seem that this question has been answered with total certainty. The popular belief is that “superbugs” in the food system are the product of industrial agriculture. The dogma is that feedlots (also called concentrated animal feeding operations or CAFOs), grain-feeding, and genetically modified organisms (GMOs) are the root cause of everything wrong in our food system including food safety problems.
For example, Michael Pollen said in a 2010 editorial, “The Food Movement Rising” (11):
“The 1993 deaths of four (sic, three) children in Washington State who had eaten hamburgers from Jack in the Box were traced to meat contaminated with E. coli O157:H7, a mutant strain of the common intestinal bacteria first identified in feedlot cattle in 1982.”
But, Dr. Thomas Whittam (1954-2008), a pioneer in the study of E. coli O157:H7 evolution, said in a 1998 paper published in Emerging Infectious Diseases (15):
“It has been proposed that an increased mutation rate (indicated by the frequency of hypermutable isolates) has facilitated the emergence of Escherichia coli O157:H7. Analysis of the divergence of 12 genes shows no evidence that the pathogen has undergone an unusually high rate of mutation and molecular evolution.”
Then in 2011, Dr. Eric Denamur, a French expert in the ecology and evolution of microorganisms, pointed out in Clinical Microbiology and Infection that the shiga toxin-producing E. coli German outbreak teaches us a lesson in genome plasticity (5):
“The main lesson from this outbreak is that we should be aware of the capacity of the E. coli species to produce new combinations of genes, leading to the emergence of highly aggressive strains. Furthermore, antibiotic pressure in human and veterinary medicine should be kept as low as possible, as it will select for such strains once they become resistant.”
So, I jumped into the literature to gain a deeper understanding of the question about the origin of E. coli O157:H7 and other STECs, especially the role industrial agriculture may or may not have played in their evolution and emergence as human pathogens. What was the ultimate answer to the question of whether STECs are old or new pathogens, and where they arose? I would have loved a clear answer, but only came up with “it depends.”
This 3-part series summarizes my findings from the literature review.
Terminology
Escherichia coli was named after its discoverer, Theodor Escherich. The current terminology and nomenclature (naming) of E. coli strains can be confusing. There are over 700 E. coli “serotypes” described. Most of these E. coli strains are harmless inhabitants of the intestinal tract of humans and other warm-blooded animals (1).
An E. coli serotype is named based on its numbered “O” (letter capital “O,” not zero) and “H” antigen types. E. coli O157:H7 is the prototype of a subset of pathogenic strains called enterohemorrhagic E. coli (EHEC). EHEC is a “pathotype” associated with human infections that may cause gastrointestinal and hemorrhagic symptoms such as bloody diarrhea and hemolytic uremic syndrome (HUS). E. coli O157:H7 and other EHEC pathotypes belong to a broader group of E. coli called shiga toxin-producing E. coli (STEC) as shown in the figure. Members of the STEC “serogroup” carry shiga toxin genes (stx1 and/or stx2). STEC strains (including E. coli O157) are found primarily in healthy animal hosts (e.g., cattle, goats, sheep, pigs, deer, elk). The harmful strains may be transmitted to humans through contaminated food, water, contact with infected animals, or person-to-person transmission via fecal-oral ingestion.
Interestingly, according to recent research in Germany (2), the E. coli O104:H4 strain linked to raw sprouts is a combination of two different pathotypes: entero-aggregative E. coli (EAEC) and EHEC. A proposed name for the new pathotype is entero-aggregative-hemorrhagic Escherichia coli (EAHEC). It is unknown if the natural reservoir of this new EAHEC type is of human or animal origin.
Bacterial Evolution
Understanding the terminology used in describing E. coli strain relationships is important in deciphering the research into STEC evolution, including how fast these strains mutate into new variants. Serotyping is based on differences in surface antigens, which are likely encoded by genes that evolve slowly. In contrast, “virulence factors” describe generally a broad group of molecules or proteins that affect the bacteria’s ability to cause disease in humans. Shiga toxins and proteins or enzymes that confer antibiotic resistance are examples of virulence factors. Virulence factors are usually encoded by genes in the bacteria’s chromosomal DNA, or genes encoded by bacteriophage or plasmid DNA carried inside the bacteria. The ability of some of these virulence factor genes to move rapidly between different populations of E. coli may explain short-term changes in the virulence potential of some strains.
In Part 2, the discovery of E. coli O157:H7 and evidence of long and short-term evolutionary changes influencing its emergence as a human pathogen will be explored. In Part 3, evidence for and against the importance of agriculture practices (e.g., feedlots, GMOs) in the spread of E. coli O157:H7 and other STECs will be reviewed. (Part 1 as PDF)
ReferencesContinue Reading Where the Hell did Shiga Toxin E. coli come from? A Literature Review – Part 1
Health Losses in the United States for Foodborne Illness are $77,000,000,000 a Year
I would argue there is no way to really value the loss at least in the human dimension.
Today I was reading Robert Scharff’s article “Economic Burden from Health losses Due to Foodborne Illness in the United Sates” in this month’s Journal of Food Protection.
Scharff’s coast analysis is based upon Centers for Disease Control
How good is your eyesight? Can you see an infective dose?
I am so tired of the emails from people – mostly people linked to the food industry – who just say, “cook it” or “wash it” and all will be good.
Say, how good is your eyesight?
Definition of Infective dose – the amount that can sicken or kill you or your kid after ingestion.
Santa got Poisoned
You can still get the book at Amazon – “Poisoned: The True Story of the Deadly E. Coli Outbreak That Changed the Way Americans Eat.”
Reviews:
“A fast-paced narrative and a cautionary tale about how public health policy, corporate practices and public relations, and lawyers’ chutzpah and frenzy for fees can converge in a
Graduates – I have one word for you – Epidemiologist
You might find this not surprising, but I read the CDC’s Morbidity and Mortality Weekly Report (MMWR) weekly. In reading this week’s article “Food Safety Epidemiology Capacity in State Health Departments — United States, 2010,” I was struck by the thought that if I had to do it all over again, I would have taken
Information as Currency in Public Health
Are we seeing an emerging trend favoring secrecy?
The 2006 E. coli O157:H7 outbreak linked to DOLE baby spinach was the known high-water mark for critical safety failures by Salinas, California’s leafy green growers and processors (1). Well over two hundred confirmed illnesses nationally, five deaths, and dozens of cases of kidney failure were the coup-de-grace for a ten-year period that saw a litany of E. coli and Salmonella outbreaks linked to Salinas’s leafy greens. But the outbreak, and more specifically the painstaking investigation and analysis that followed, also marked the beginning of the end of full disclosure, and the beginning of, in some cases, complete silence by some state and federal public health officials about the details and even existence of foodborne illness outbreaks.
The 2006 Spinach E. coli outbreak was, of course, a highly public event, no doubt requiring an open and frank discussion of the actions and failures that contributed to so many illnesses and deaths. Together with the Food and Drug Administration (FDA), California’s Food Emergency Response Team (CalFERT), which was a collection of epidemiologists and other scientists formed in 2005 to investigate outbreaks originating in California, produced a lengthy report discussing the trail of evidence that lead to the conclusion that DOLE’s baby spinach caused the outbreak, as well as the microbiological and environmental findings that gave some insight into the outbreak’s cause and likely source (2).
After the 2006 Spinach outbreak—in fact, within three months of it—two more E. coli outbreaks, which sickened at least 152 people in six states, were linked to lettuce produced by California growers (3, 4). Again, CalFERT investigated the outbreaks and issued final reports, thereby providing both the industry and the public generally with information about the state of the industry in America’s salad bowl, and most importantly, the likely causes of the outbreaks.
But there the paper trail slowed. Since the devastating fall of 2006—three outbreaks; 404 illnesses; five deaths; dozens of cases of kidney failure—CalFERT has not issued a single report of its investigative activities, despite a leafy-green link to many more outbreaks. And, these are only the outbreaks that are known to have occurred. Moreover, what can be pieced together based on limited responses to Freedom of Information requests, shows that the trend is not only limited to a lack of documented investigative conclusions about an outbreak, but also incomplete investigation of outbreaks, and increasing failures to notify the public at all that an outbreak has occurred. A few of the more known examples:
• September 2008—at least 45 residents of Michigan, Illinois, and Ontario, Canada were infected by E. coli contaminated iceberg lettuce that was grown in California and processed at Aunt Mid’s Produce Company, a Detroit-area wholesale distributor. Again, neither the FDA nor CalFERT issued any kind of a summary report documenting their conclusions about the source or cause of the outbreak (5).
• April 2010 – at least 33 residents of Michigan, Ohio, Tennessee, Pennsylvania, and New York were sickened by a relatively rare strain of E. coli called E. coli O145. Perhaps the most publicly known outbreak since the devastating fall of 2006, FDA refused to name the company that had grown the lettuce, instead choosing to identify only the state where the farm was located: Arizona. CalFERT was not involved in this investigation (6A, 6B).
• October 2011 – at least 60 people from 10 states were sickened by E. coli contaminated romaine lettuce. Most of the ill were customers of Schnuck’s grocery stores in Missouri. Traceback investigation revealed both the processor of the contaminated lettuce and the grower, but again the FDA has declined to name either company (7).
A few of the lesser known, or not publicized, examples:
• May 2008—at least 10 residents of Washington State were infected by E. coli contaminated romaine lettuce grown and processed in Salinas, California. Despite being involved in the investigation and product traceback to the lettuce processor, neither the FDA nor CalFERT documented their findings about the outbreak’s source or cause (8).
• October 2008 – at least 55 people in Canada, California, North Dakota, Illinois, Florida, New Jersey and Ohio were sickened by E. coli-contaminated romaine lettuce that had been grown in California. California and FDA investigation revealed that the implicated lettuce had been supplied to retail locations where people became ill by a Salinas, California company. Again, neither CalFERT nor the FDA issued a summary report about the outbreak (9).
• July/August 2009 – dozens of Oregon, Washington, Idaho, Colorado, and Montana residents, and multiple Canadians, were sickened by Salmonella Typhimurium in an outbreak dubiously investigated by officials at the California Department of Public Health’s Food and Drug Branch. The contaminated lettuce was grown and processed in Salinas, California, and despite clear epidemiological evidence implicating the lettuce, California officials declined to state a relationship between the implicated lettuce and the outbreak. Neither California nor the FDA issued a comprehensive report on the outbreak, nor was the implicated product ever recalled (10).
• September 2009 – at least 19 residents of Colorado, Utah, New York, South Dakota, Wisconsin, and North Carolina were infected by E. coli contaminated lettuce grown in Salinas, California. Again, neither CalFERT nor the FDA generated a report on outbreak findings (11).
• September 2009 – 10 individuals in 6 different states, Colorado, Connecticut, Iowa, Minnesota, Missouri, and North Carolina suffered E. coli infections, sharing an indistinguishable PFGE pattern. The outbreak was identified by the CDC as cluster 0910MLEXH-1. Epidemiological investigations by multiple states strongly suggested lettuce as the source of the outbreak. The lettuce served at a restaurant in Colorado where both Colorado members in the outbreak consumed lettuce was traced to a specific grower in California’s Salinas Valley. Colorado state health officials pushed for further Federal agency effort but were rebuffed:
By mid-October, Colorado had not received any further communication from the CDC and FDA about the traceback, so Colorado made several inquiries about the status of the investigation. Investigators from the CDC reported that FDA had decided not to pursue further traceback activities because of limited resources and the length of time that had elapsed since the original exposures with no new cases. Colorado challenged this decision, but FDA did not change its position about pursuing traceback further (12).
Since the fall of 2006, and the media vortex that the three large E. coli outbreaks that occurred then created, the FDA and CalFERT have repeatedly failed to provide conclusions, and in some cases much information at all, about multiple major public health crises that have occurred in this country. This is a threat to the public’s health, which has as its only currency the free and rapid exchange of information.
Questions raised by FDA’s and CalFERT’S approach, or lack thereof, to providing information to the public about post-2006 leafy green outbreaks are many. Is funding for public health programs lacking? Across the board, possibly, but CalFERT has not experienced any cuts to its operating budget; in fact, during this period, CalFERT has received a large grant from FDA. If not a problem of funding, will CalFERT and FDA respond that they lack manpower? Unlikely, given the underlying reasons for the existence of CalFERT in the first place, which was a specific devotion of resources and highly competent public health officials to the problems emanating from Salinas Valley, and California generally. There is no clear conclusion available from the known data as to why there is a lack of complete disclosure. Of course, there has been no explanation from these public health bodies regarding their reasons for the trend of non-disclosure.
Whatever the explanation, the lack of information about these outbreaks is far from simple instances of non-disclosure. Indeed, the path that CalFERT and FDA have chosen to take since the fall of 2006 threatens a general withdrawal from the obligations of open disclosure. And, this is only about the outbreaks that are known. There are likely many more that have occurred that have never seen the light of any disclosure at all.
References:Continue Reading Information as Currency in Public Health