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How Escherichia coli 0157:H7—Cause of Ongoing Contaminated Spinach Outbreak—Poisons Humans

Biot Report #408: October 01, 2006

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German pediatrician named Dr. Theodor Escherich (1857-1911) first identified Escherichia coli, a small rod-shaped germ, in 1884 when he examined human excrement under his microscope. E.coli is always present in the feces of healthy humans. Most E.coli do not cause disease in human beings. (1) E. coli comes in many different strains, which can be divided in many subgroups, referred to as serotypes. The principal serotypes are defined by chemicals on the surface of the germ known as O antigens and subdivided into serotypes on the basis of other structural variations, such as the H antigens. (2)

Investigators in 1982 discovered a previously unrecognized strain of E.coli associated with two human outbreaks of illness characterized by severe, crampy abdominal pain; watery diarrhea followed by grossly bloody diarrhea; and little or no fever. (3-4) The first outbreak occurred in Oregon between February and March 1982 and the second one occurred in Michigan in May and June 1982. A total of 47 people were affected. The strain of E.coli causing the illness was E.coli 0157:H7. The epidemiological investigation uncovered the source of the E.coli 0157:H7 in hamburger meat served at outlets of the same fast food chain (McDonalds) in both outbreaks. (4)

Interestingly, earlier in 1977 Canadian researchers had discovered that certain strains of E.coli—H10401, H10407, B7A, and B2C, among others (but not including 0157:H7, which was not tested)—elaborated a newly-identified toxin (poison) that killed “Vero” cells in a culture dish. Vero cells are a tissue culture line established from the kidneys of an African Green Monkey. (2,5) The toxin isolated by researchers from the E.coli H10401, H10407, and so on was similar to the toxin produced by another germ called Shigella dysenteriae, which also causes severe bloody dysentery, just like E.coli:0157:H7. Because of the similarity of the two toxins, the E.coli toxin was called “Shiga-like” toxin, and later, “verotoxin” or “verocytotoxin” (kills vero cells).

Not long after the 1982 two-state outbreak described above, researchers determined that all E.coli 0517:H7 strains associated with outbreaks of dysentery produce verotoxin. (6) Sometimes this group of E.coli 0517:H7 strains are called “Shiga-toxin-producing E.coli” or STEC. (2)

How Verotoxin Injures Humans

When humans ingest E.coli 0157:H7 germs embedded in foods such as contaminated ground beef or fresh green leafy vegetables, the germs move down the esophagus into the stomach and then to the intestines. The E.coli 0157:H7 germ is remarkably resistant to stomach acid, and is therefore not easily killed there. Furthermore, a very small number of this germ is needed to cause harm to the human body, similar to Shigella dysenteriae germs, which also secrete a toxin similar to verotoxin, as noted above. At some point the Shigella and E.coli germs must have exchanged their nuclear material.

The human intestine has a mucous lining that is called a “brush border”. The verotoxin elaborated by the E.coli 0157:H7 attaches (binds) to the brush border and dissolves the delicate little projections or “fingers” called microvilli that project into the intestinal tunnel. In healthy humans, across these microvilli flow nutrients from food in the intestines into the bloodstream. From there the blood carries the nutrients to hungry cells throughout the body.

Unfortunately, in the diseased human smitten with E.coli 0157:H7 dysentery, the germ reproduces and while multiplying elaborates verotoxin that eats away at the cells of the microvilli of the brush border. After sufficient verotoxin is produced, the erosion extends into one or more blood vessels that normally run through the wall of the intestine. These blood vessels then bleed into the intestinal lumen, which is why some people with E.coli:0157:H7 dysentery have bloody diarrhea (the blood continues down the intestines to the anus, where it is expelled). People in whom the wall of the intestine has been damaged in this way have “hemorrhagic colitis”. The World Health Organization is calling E.coli:0157:H7 “enterohemorrhagic E.coli” or EHEC. (7) Other terms currently in use for E.coli:0157:H7 are “verocytotoxin-producing Escherichia coli”, “verotoxigenic Escherischi coli”, and VTEC. (2)

Some people afflicted with E.coli 0157:H7 food poisoning experience only watery diarrhea (no blood), which means the verotoxin that was elaborated by the germs did not erode into blood vessels in a substantial way. Other people afflicted with VTEC food poisoning experience first watery, then bloody, diarrhea. In this group of people, the verotoxin definitely eroded into some blood vessels in the lining of their intestine. If people in this group are fortunate, the disease process stops after the bloody diarrhea, which is bad enough, and they recover without further sequelae within a couple of weeks. Up to 95% of all people sickened with VTEC go on to full resolution of their symptoms. The other 5% or so of afflicted people are not so fortunate.

Hemolytic-Uremic Syndrome

In 5%-30% of people infected with VTEC, especially children (median age: 4 years), the disease process does NOT stop with bloody diarrhea. (2) Rather, it progresses to a life-threatening syndrome called the “hemolytic-uremic syndrome” or HUS about one week after the onset of diarrhea. In this group of people, the verotoxin damages the lining of the blood vessels, called the “endothelium”. Platelets and fibrin traveling around in the bloodstream migrate to the site of blood vessel wall “perturbation” to repair the damage. But something goes amiss at this point, and pathologic clumps of fibrin and platelets—immune complexes—form independently of the vessel wall repair process. The immune complexes then race around the blood stream, slicing up healthy blood cells in the process, once described as “throwing a tomato through chicken wire” (2a) and completely or partially occluding tiny blood vessels in very important organs, such as the kidneys and brain, causing organ failure.

Platelets are used up (consumed) in these immune complexes, resulting in a low platelet count, which is called “thrombocytopenia”. Red blood cell count decreases, too, resulting in anemia. As many as 50% of people with HUS secondary to VTEC require short-term dialysis (couple of weeks) until their kidneys recover. (2)

If renal failure is managed properly with dialysis, most patients experience recovery in a matter of weeks although some patients (up to 11% in one study) go on to develop degrees of chronic renal failure. (8) Because of the blockages in the blood vessels and bleeding tendencies because of low platelets, some people with HUS develop neurological problems (problems with the brain and nervous system). Between 3 and 5% of people with HUS die from their disease. (9-10)

Thus, the constellation of clinical findings of hemolytic-uremic syndrome includes anemia (microangiopathic hemolytic type), thrombocytopenia, and renal failure. (11) HUS of course has many causes, but currently a major cause, especially in children under 16 years of age, is E.coli 0157:H7. In fact, according to one study conducted by the Centers for Disease Control and Prevention (CDC) between 1997 and 1999, 123 cases of HUS among the pediatric population were identified, and of these 123 cases, 53% were caused by E.coli 0157:H7. Of these 123 children sick with HUS, 13 (11%) died and 17% had neurologic problems at discharge. (10) People with HUS are as sick as people get.

Children are not the only group that is particularly susceptible to the verotoxin-elaborated by E.coli 0157:H7. The elderly do not do tolerate it well either. A major outbreak of VTEC occurred in Scotland in December 1996 and January 1997, with over 400 people infected and 20 deaths. The majority of the dead were elderly citizens who succumbed after eating meat at a lunch for retirees at a church in Wishaw, Scotland. A chronology for that event is available at an interesting website maintained by an HUS family who lost a child to the disease. (11)

Thrombotic Thrombocytopenic Purpura (TTP)

In addition to HUS, another condition may result from infection with VTEC is thrombotic thrombocytopenic purpura (TTP). Adults poisoned with VTEC are more likely to develop this condition than children. TTP causes tiny blood vessels to bleed into the skin and mucous membranes because of the marked decrease in platelets. Adults with TTP will often have fever and neurological symptoms.

Where Does E.coli 0157:H7 come from?

E.coli 0157:H7 disease is a zoonosis, meaning it is a disease that is communicable between animals and humans under natural conditions. Livestock are a reservoir for most VTEC, with cattle being the principal source. In one study, VTEC was isolated in 752 of 4,800 cattle (15.7%). VTEC is also found in the intestines of sheep, goats, deer, horses, dogs and cats. Seagulls, pigeons and geese are also known to carry the germ. Cattle do not become sickened by the germ because the verotoxin is unable to attach to receptors on the microvilli of the bovine intestine. Thus, the germs colonize the gut but do not invade the gut wall.

When cattle feces containing the E.coli 0157:H7 germ pass into water used for, say, irrigation, the germ can contaminate crops, such as leafy vegetables (lettuce and spinach), which have a broad surface area and grow close to the ground where they may come into contact with the water containing VTEC. Other ways of VTEC food contamination is via animal fecal material transferred into milk at the time cows are milked, onto vegetables when manured (fertilized with manure containing VTEC), and onto carcasses at carcass dressing (feces stuck to the animal hides or failure to close off adequately the esophagus and anus during evisceration). The prime risk foods are undercooked beef burgers, unpasteurized or recontaminated pasteurized milk and cheese, and raw vegetables. (2) Heating foods well kills VTEC even as freezing and application of acid does not.

Person to Person Spread Does Occur; Flies Spread It, Too

VTEC is efficiently transferred from an infected person to a non-infected person, unfortunately. Laboratory staff have become infected with VTEC while working with the organism. This occurrence has led to the categorization of VTEC as a Hazard Group 3 organisms requiring Containment Level 3 laboratory facilities. (2)

In addition, flies that breed in feces and other organic refuse (filth flies) are now known to be vectors of VTEC. “The potential role of filth flies in the epidemiology of [VTEC] in the United States was investigated by examining the prevalence of [VTEC in flies] from two Arkansas turkey facilities.” (12) Culturing verified that the flies were carrying viable VTEC. House flies and black dump flies associated with poultry efficiently carried VTEC as well.

Summary

E. coli 0157:H7 came out of the blue in 1982 and is rapidly emerging as a major public health hazard capable of causing very high morbidity and some deaths, especially in the young and old. The transmission characteristics of the infection make it a very high priority for public health policy.

Sources:

1. SEMP Biot #109: “Who Is Dr. Theodor Escherich?” (August 21, 2004) available at: http://www.semp.us/biots/biot_109.html; accessed September 30, 2006. See also “Aurora’s Boil Order: The Local Public Health Perspective” in Securitas (March 2004), Vol. 3, No. 2 available online at: http://www.semp.us/securitas/2004mar.htm; accessed September 30, 2006.

2. Food Authority of Ireland: “The prevention of E.coli 0157:H7 infection: A shared responsibility.” 1999, p. 1. See: http://www.irishscientist.ie/P69.htm; accessed September 30, 2006.

2a. “Hemolytic-Uremic Syndrome” at: http://www.medicinenet.com/hemolytic_uremic_syndrome/article.htm; accessed September 30, 2006.

3. LW Riley, RS Remis, SD Helgerson, HB, et al: “Hemorrhagic colitis associated with a rare Escherichia coli serotype.” In “New England Journal of Medicine” (1983) 308:681-685.

4. JG Wells, BR Cavis, K Wachsmuth, et. al: “Laboratory investigation of hemorrhagic colitis outbreaks associated with a rare Escherichia coli serotype” in “Journal of Clinical Microbiology” September 1983, pp 512-520. Available online at: http://www.pubmedcentral.gov/tocrender.fcgi?action=archive&journal=81; accessed September 30, 2006.

5. J Konowalchuk, JI Speirs, S Stavric: “Vero response to a cytotoxin of Escherichia coli.” In “Infection and Immunity”, Dec. 1977, pp 775-779. Available at: http://www.garfield.library.upenn.edu/classics1992/A1992JG65800001.pdf#search='Vero%20response
%20to%20a%20cytotoxin%20of%20Escherichia'; accessed September 30, 2006.

6. F Gunzer, H Bohm, H Russmann, et al: “Molecular detection of sorbitol-fermenting Escherichia coli 0157 in patients with hemolytic-uremic syndrome.” In Journal of Clinical Microbiology, July 1992, pp. 1807-1810.

7. World Health Organization, Codex Alimentarius Commission, Food and Agriculture Organization of the United Nations, “Joint FAO/WHO Food Standards Programme Codex Committee on Food Hygiene, Thirty-Fifth Session, Orlando, USA, 27 January – 1 February 2003: “Risk profile for enterohemorrhagic E.coli including the identification of the commodities of concern, including sprouts, ground beef and pork.” CX/FH03/5-Add.4, September 2002. Available online at: ftp://ftp.fao.org/codex/ccfh35/fh0305de.pdf; accessed September 30, 2006.

8. Ramzi Cotran, Vinay Kumar, Stanley Robbins: “Robbins Pathologic Basis of Disease”, 5th Edition, 1994, pp. 619-620 and 980-981.

9. HUS was defined in one study spanning 1997 to 2001 as: “1) acute renal failure, including oligoanuria and elevated creatinine level for age, 2) microangiopathic hemolytic anemia (hemoglobin level <10 g/L with fragmented erythrocytes), and 3) thrombocytopenia (platelet count <130,000 × 109/L) in the absence of septicemia, malignant hypertension, chronic uremia, or primary vascular disease. Diarrhea-associated HUS was defined as disease that immediately followed diarrhea or bloody diarrhea. Nondiarrhea-associated HUS was defined as disease in which ≥1 episodes did not follow an episode of diarrhea.” See:

Richard M. Lynn, Sarah J. O'Brien, C. Mark Taylor, et al: “Childhood Hemolytic Uremic Syndrome, United Kingdom and Ireland” in “Emerging Infectious Diseases” April 2005, Vol. 11, No. 4. Available online at: http://www.cdc.gov/ncidod/EID/vol11no04/04-0833.htm; accessed September 30, 2006. This paper has a very good reference list.

10. E Dunne, D Wallace, J Bender, et al: “Results from 3 y ears of active surveillance for Hemolytic Uremic Syndrome (HUS) through FoodNet, United States, 1997-1999. Abstracts of the Infectious Diseases Society of America, 38th Annual Meeting, New Orleans, LA, September 2000. Available online at:

http://www.cdc.gov/foodborne/publications/54_dunne_2000.pdf; accessed September 30, 2006.

11. “Eric’s Echo, the Scottish Outbreak” available at: http://www.ericsecho.org/scottish.htm; accessed September 30, 2006.

12. AL Sazlanski, CB Ownes, T McKay, et al: “Detection of Campylobacter and Escherichia coli 0157:H7 from filth flies by polymerase chain reaction” in “Medical and Veterinary Entomology”, vol. 18, issue 3, p. 241, September 2004. Available online at: http://comp.uark.edu/~aszalan/med_vet_ent_2004.pdf#search='detection%20of%20
campylobacter%20and%20escherichia'; accessed September 30, 2006.