Escherichia coli, usually abbreviated to E. coli, discovered by Theodor Escherich, a pediatrician and bacteriologist, is one of the main species of bacteria that live in the lower intestines of warm-blooded animals, including birds and mammals. They are necessary for the proper digestion of food and are part of the intestinal flora. Its presence in groundwater is a common indicator of fecal contamination. The name comes from its discoverer, Theodor Escherich. It belongs among the Enterobacteriaceae, and is commonly used as a model organism for bacteria in general.
- When the bacteria get out of the intestinal tract and into the urinary tract, they can cause an infection sometimes referred to as "honeymoon cystitis" because intercourse can lead to introduction of bacteria into the bladder. Although it is more common in females, urinary tract infection is seen in both males and females. It is found in roughly equal proportions in elderly men and women. Since bacteria invariably enter the urinary tract through the urethra, poor toilet hygiene can predispose to infection but other factors are also important (pregnancy in women, prostate enlargement in men) and in many cases the initiating event is unclear. Anal sex is also a risk factor for males.
- When the bacteria get out of the intestinal tract through a perforation (a hole or tear, which could be caused by an ulcer, for example) and into the abdomen, they usually cause an infection called "peritonitis" that can be fatal. However, E. coli are extremely sensitive to antibiotics such as streptomycin or gentamycin, so treatment with antibiotics is usually effective.
- Certain strains of E.coli are toxigenic (some produce a toxin very similar to that seen in dysentery) and can cause food-poisoning usually associated with eating contaminated meat (contaminated during or shortly after slaughter or during storage or display). Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. E. coli can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, is highly similar in structure and function to Cholera toxin. It contains one 'A' subunit and five 'B' subunits arranged into one holotoxin. The B subunits assist in adherence and entry of the toxin into host intestinal cells, where the A subunit is cleaved and prevents cells from absorbing water, causing diarrhea.
Some strains of Escherichia coli have surface antigens analogous to the human blood group ABH antigens, and that these are carbohydrates associated with membrane lipopolysaccharides. This study has demonstrated that E. coli strains Y1089 and Y1090 possess the H antigen of blood type O, which can also be converted to the A antigen, again illustrating how by converting one blood type antigen into another gut bacteria can produce opposing blood type 'immunization' and cause digestive intolerance. ()
The really dangerous variant of E .coli bacteria (called 'O157:H7') was first recognized as a cause of human disease in 1982. Large outbreaks of E. coli O157:H7 have been reported in the United States, including an outbreak in 1993 linked to undercooked hamburgers that resulted in more than 600 reported cases and 4 deaths. In 1996, more than 6000 schoolchildren in Japan developed E. coli O157:H7 infection from eating contaminated radish sprouts. Though vegan enthusiasts tend to emphasize meat as a cause of E. coli infection, since 1995 rew sprouts have been associated with 13 outbreaks of food borne disease due to E. coli or Salmonella. Contamination of the sprouts themselves rather than improper handling, is believed to be the source of the problem.
In most cases the infection is limited to diarrhea and cramps, although in advanced cases the diarrhea can be bloody and debilitating. In fewer than 2% to 7% of those infected, particularly in the very young and the very old, a disorder called Hemolytic uremic syndrome (HUS) will develop. A bacterial toxin damages small blood vessels in the kidney, reduces platelet counts, and destroys red blood cells. Kidney function can be greatly reduced to the degree that dialysis may be necessary. There are no currently available treatments that can prevent HUS once a person is infected with the organism.
It appears that many of the variants of E. coli have developed individualized tastes for different ABO blood types. Even their strategies differ from blood type to blood type:
Attachment -Type A: Many of the bad forms of E. coli express rope-like bundles of filaments, termed bundle-forming pili (BFP). Which allow them to attach to the lining of the intestines. These 'bad' E. coli have suction-cup like lectins on their pili that attach to the various sugars (glycoproteins or glycolipids) comprising the polysaccharides of the intestinal mucus lining. Many of these sugars are in fact, particular ABO antigens. For example, certain E. coli strains which colonize the human digestive tract express lectins specific for different glycolipids called a 'globoseries.' One such glycolipid, globo-A, is restricted to individuals of blood group A with a positive secretor state. ()
Mimickry- Types B and AB: It appears that many forms of E. coli capable of causing diarrhea are immunologically 'B-like'. That is, they possess an antigen on their surface which resembles the antigen which conveys 'type B blood.' Several studies show a higher number of type B and AB people (who cannot manufacture anti-B antibodies) being afflicted with E. coli caused gastroenteritis. In one study, 148 Egyptian patients were studied for parasitic and bacterial infections in relation to ABO blood groups. There was a 'significant relationship' between blood group B and an excess among cases of E. coli (46.15%). The expected frequency of type B should have been around 11%. ()
It has been hypothesized for years that the reason certain individuals manufacture antibodies to opposing blood types is a result of 'inapparent immunization' by bacteria antigens in the gut. The hypothesis that naturally occurring anti-B (in those individuals who are type O or type A blood) protects against type B like E . coli infection was verified in a second study () which looked at the blood groups of 115 patients with E. coli infection and compared these with three "control" populations: 138 patients with infection due to other organisms; 23,135 hospitalized patients; and 40,038 normal blood donors. The incidence of B and AB blood types , (who cannot make anti-B antibodies) in the E. coli infection group was significantly higher than A and O blood types (who can make anti-B antibodies).
Interaction- Type O: There is an association of type O blood with the severity of the diarrhea that results from E. coli infection. During studies of diarrhea due to Escherichia coli in 316 adult volunteers, ABO and Rh blood group determinations were done to look for differences in the severity of illness in association with certain blood groups. Volunteers with O blood group had a significantly higher attack rate for diarrhea than persons with other blood groups. (). The authors in this case speculated that there was an interaction between the type O blood group substance and the toxin produced by the bacteria.
Though certainly no substitute for avoidance, infection with E. coli might at least result in one positive outcome: People recovering from E. coli enteritis apparently have higher levels of anti-Thomsen Friedenreich (TF) antibodies. The TF antigen is often expressed in cancer cells, so perhaps an E. coli infection might protect against certain cancers.
Blood group and susceptibility to disease caused by Escherichia coli O157
J Infect Dis. 2002 Feb 1;185(3):393-6. Epub 2002 Jan 8.
Blackwell CC, Dundas S, James VS, Mackenzie DA, Braun JM, Alkout AM, Todd WT, Elton RA, Weir DM.
- Patients (n=186) infected during the Escherichia coli O157 outbreak in Scotland in 1996 were assessed for blood group markers (ABO, Lewis, and P) associated with other gastrointestinal infections. Binding of bacteria to epithelial cells was assessed by flow cytometry. Buffy coats from blood donors were examined for inflammatory responses to culture filtrates of the outbreak strain. Individuals of blood group O comprised 63.4% of patients, compared with 53.4% (P <.05) and 53.9% (P <.01) of neighboring populations in Airdrie and Glasgow, respectively; group O also comprised 64.3% of patients with hemolytic uremic syndrome (HUS) and 87.5% of patients who died (P <.05). No or weak agglutination by anti-P antiserum was observed for 40.7% of control persons (n=122), 61.5% of all patients (P =.0027), and 83.3% of patients with HUS (P =.013). The susceptibility of group O to E. coli was not associated with increased binding of bacteria to epithelial cells or with higher production of [Tumor Necrosis Factor (TNF)? tumor necrosis factor (TNF)-alpha] or interleukin-6. Leukocytes of P-negative blood donors produced higher levels of TNF-alpha than those of P-positive donors.