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Some frequently asked
questions about E. coli:


Q: What is Escherichia coli, or E. coli?

A: E. coli are common, normally benign intestinal bacteria found in humans and animals, but the O157:H7 strain produces a powerful toxin that can cause bloody diarrhea, abdominal cramps and in some cases death. The O157 bacteria is virulent and tough and only a few are needed to cause illness.

 

Q: How is E. coli O157:H7 spread?

A: The O157 strain is not naturally present in humans, but does occur in cattle. Infected animals can spread the bacteria through their feces, which can wind up on beef during the butchering process. Eating undercooked ground beef causes most E. coli-related illnesses. Feces-contaminated water, vegetables and fruit, as well as unpasteurized milk or juice, can also cause infection.

 


Q: What illness does E. coli O157:H7 cause?

A: The O157 strain can cause bloody diarrhea and dehydration. The very young, seniors and people with weak immune systems are the most vulnerable. In children, O157 may lead to a severe, sometimes fatal kidney disease called HUS (hemolytic-uremic syndrome).

 

Q: How is E. coli O157:H7 infection diagnosed?

A: The O157 strain often goes undiagnosed because many labs don't test for it. Anyone who suddenly has diarrhea with blood should be tested.

Q: How is the illness treated?

A: This is an antibiotic-resistant strain of E. coli. Most people recover without treatment in 5-10 days.

 

Q: What are the long-term consequences of infection?

A: People who only have diarrhea usually recover completely. About a third of people with HUS can have kidney problems years later, and some require long-term dialysis.

Sources: Centers for Disease Control

 


OPINION
San Francisco Chronicle

Fighting E. coli the old-fashioned way

by Jeff D Leach Paleobiotics Lab

In the wake of E. coli 0157:H7 outbreaks associated with spinach and other produce in 2006, the new 110th Congress will be dusting off and reintroducing the Food Safety Act (S. 729), initially proposed in 2005 by Senator Dick Durbin (D-IL), to assure the American public that the government is working hard to substantially reduce future food-borne outbreaks.

Unfortunately, this well-intended legislation will fall short of anything meaningful, as its patrons most certainly fail to understand the basic evolutionary rules of the germ warfare raging in the American gut and the bigger challenges facing the populace in this biological arms race.

As executives of the produce industry hit hardest by the illness and deaths attributed to E. coli 0157:H7 in 2006 brace for a possible onslaught of new regulations and additional inspectors trudging about their fields and packaging plants, they need only look out to the fields beyond their office windows to see a better solution to what ails them and the American public.

Among the lush greens, yellows and reds of the American produce landscape, lies a simple, but critical component, to our evolutionary success as a species and the best defense we have ever had – or will likely ever have – against reducing our risk from E. coli 0157:H7 and the assortment of pathogens that seek to do us harm on the biological battle field that is us.

The simple defense to be found amid these fields is good old dietary fiber.

As you read this, there are trillions of tiny microbes (including billions of harmless strains of E. coli) living throughout your continuous gastrointestinal tract – from mouth to anus. These tiny evolutionary hitchhikers have been with you every minute of every day from the moment you entered this world and will be so until you die. And then they will eat you. But that’s the good news.

The bad news is our so-called modern diet of highly processed fiber poor grains, in addition to added sugars and fats, is literally starving our “friendly” bacteria and putting us at increased risk. The friendly bacteria in our bodies are the first line of defense against invading pathogens, such as E. coli 0157:H7. Like any good soldier they require nutrients to fight the good fight and dietary fiber is an important part of that nutrient base.

Simply stated: Fiber is not food for us, it’s food for bacteria that live in our gut.

Our not-so-distant ancestors regularly consumed between and often more than 50 and 100 grams of dietary fiber from diverse sources every day. This is the nutritional reality upon which our modern genome was selected and the symbiotic relationship which the trillions of bacteria in our gut evolved to depend upon.

However, the average American today consumes about 12 to 15 grams a day – roughly half of what the government recommends and only a fraction of what our gut bugs need in order to resist infection and disease caused by a steady stream of pathogenic bacteria and viruses that enter our gut every day.

No amount of government oversight will ever completely remove the threat of pathogens in our food supply. There are too many variables from plough to plate – not to mention that the bad bugs have us out numbered.

While a cleaner and safer food supply has allowed our species to maintain mammalian dominance, we must not lose sight of the delicate nutritional requirements of our friendly gut bugs and the indispensable role they play in our tenuous existence on this microbe-dominated planet.

The health implications of our staggering drop in consumption of dietary fiber has opened the door to E. coli 0157:H7 and its band of pathogenic brothers who make millions of people sick every year, sending hundreds of thousands to the emergency room with diarrhea, bloody diarrhea, intestinal cramping, and fever, and sending an increasing number of us, to the morgue.

The important symbiotic relationship we share with our friendly microbes and their role in our natural resistance to infection should be taking center stage in the upcoming Congressional hearings on how to best protect “the people” from the inevitable food-borne pathogens associated with produce, and specifically, how to deal with this monster E. coli 0157:H7.

The recent outbreaks have understandably made the American public skittish not only about spinach and other produce tainted with E. coli 0157:H7, but about produce in general. This may pave the way for an additional decrease of fiber in the American diet, resulting in poorer gut health and reduced ability to resist infectious agents.

The media attention given to E. coli 0157:H7 in 2006 has once again raised the awareness of deadly pathogens in our environment. This may be an opportunity, though tragic in its realization, for industry and the government to highlight the importance of increasing fiber intake via fruits and vegetables. Current government health messages to do so have had little success. Maybe it’s time to change the message.

For E. coli 0157:H7 specifically, stimulating the growth of a group of healthy bacteria in the human gut known as bifidobacterium by consuming special prebiotic dietary fibers known as oligosaccharides – found in plants such as onions, leeks, garlic, chicory, and artichokes – can fortify our natural resistance.

Bifidobacteria exert powerful effects against pathogens through competition for colonization sites and nutrients in the gut, acid excretion and antimicrobial peptides. If properly fed and stimulated, these bacteria will do their evolutionary job and make life a living hell for invading pathogens.

Interestingly, bifidobacterium dominate the gut of breast fed babies, but are known to decrease significantly as people get older. This may explain that even though a number of age groups were sickened during the 2006 outbreaks, two out of three of the deaths were elderly women. The third was a 2 year old boy. A similar pattern was seen in a deadly outbreak in Scotland in 1986 that affected hundreds and killed 20. All deaths were among the elderly.

At a time when researchers are finally acknowledging that nearly 20% of all cancers are caused by infection – up from zero just a few decades ago – and with hints that infection may play a causal role in such big time killers as breast cancer and atherosclerosis, it may be time to start asking who or what opened the pathogens door.

Ignorance of evolutionary biology and the nutritional landscape upon which humans and our microbes evolved should not preclude lawmakers and industry from exploring the role of dietary fiber in reducing our casualties in this evolutionary arms race. Continuing to ignore this simple and easy-to-implement strategy will only result in further human suffering.

I, for one, will be having a salad tonight.


*Comments about this article would be most welcome (E-mail).


Further Reading

Mixed culture fermentation studies on the effects of synbiotics on the human intestinal pathogens Campylobacter jejuni and Escherichia coli.
Anaerobe. 2003 Oct;9(5):231-42.

Pathogen survival in the external environment and the evolution of virulence. Biol Rev Camb Philos Soc. 2004 Nov;79(4):849-69. Review.

Evolutionary perspective on dietary intake of fibre and colorectal cancer. Eur J Clin Nutr. 2007 Jan;61(1):140-2.

Shiga toxin of enterohemorrhagic Escherichia coli type O157:H7 promotes intestinal colonization. Proc Natl Acad Sci U S A. 2006 Jun 20;103(25):9667-72.

Carbohydrate preference, acid tolerance and bile tolerance in five strains of Bifidobacterium. J Appl Microbiol. 2006 Apr;100(4):846-53.

Cochran, Gregory M. "Infectious Causation of Disease: An Evolutionary Perspective" Perspectives in Biology and Medicine - Volume 43, Number 3, Spring 2000, pp. 406-448

Evolutionary health promotion. Prev Med. 2002 Feb;34(2):109-18. Review.

Human Evolution, Nutritional Ecology and Prebiotics in Ancient Diet. Bioscience & Microflora Vol. 25, No. 1. pp 1-8

"Children on the frontline against E. coli": typical hemolytic-uremic syndrome. Clin Lab Sci. 2005 Spring;18(2):90-9.

Prevalence and risk factors of genital Chlamydia trachomatis infection. Medicina (Kaunas). 2006;42(11):885-94. Review.

Introducing inulin-type fructans. Br J Nutr. 2005 Apr;93 Suppl 1:S13-25. Review.

Non-toxic potentiation of cancer radiotherapy by dietary oligofructose or inulin. Anticancer Res. 2002 Nov-Dec;22(6A):3319-23.

Inulin/oligofructose and anticancer therapy. Br J Nutr. 2002 May;87 Suppl 2:S283-6. Review.

The association of Helicobacter pylori infection with the development of gastroesophageal reflux disease (GERD). J Egypt Public Health Assoc. 2001;76(3-4):265-79.

 

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