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Escherichia coli

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"E. coli" redirects here. For the protozoan parasite, see Entamoeba coli.
Escherichia coli

Scientific classification

Gamma Proteobacteria
E. coli

Binomial name
Escherichia coli
(Migula 1895)
Castellani and Chalmers 1919

Escherichia coli (pronounced /rki kola/) (E. coli), is a bacterium that is

commonly found in the lower intestine of warm-blooded animals. Most E. coli strains are
harmless, but some, such as serotype O157:H7, can cause serious food poisoning in
humans, and are occasionally responsible for costly product recalls.[1][2] The harmless
strains are part of the normal flora of the gut, and can benefit their hosts by producing
vitamin K2,[3] or by preventing the establishment of pathogenic bacteria within the
E. coli are not always confined to the intestine, and their ability to survive for brief
periods outside the body makes them an ideal indicator organism to test environmental
samples for fecal contamination.[6][7] The bacteria can also be grown easily and its
genetics are comparatively simple and easily-manipulated, making it one of the best-

studied prokaryotic model organisms, and an important species in biotechnology. E. coli

was discovered by German pediatrician and bacteriologist Theodor Escherich in 1885,[6]
and is now classified as part of the Enterobacteriaceae family of gamma-proteobacteria.[8]


1 Strains
2 Biology and biochemistry
3 Normal Role
4 Role in disease
o 4.1 Virulence properties
o 4.2 Gastrointestinal infection
4.2.1 Epidemiology of gastrointestinal infection
o 4.3 Urinary tract infection
5 Laboratory diagnosis
6 Antibiotic therapy and resistance
o 6.1 Beta-lactamase strains
7 Phage therapy
8 Vaccination
9 Role in biotechnology
10 Model organism
11 See also
12 References
13 External links
o 13.1 General

13.2 Databases

[edit] Strains

Model of successive binary fission in E. coli

A strain of E. coli is a sub-group within the species that has unique characteristics that
distinguish it from other E. coli strains. These differences are often detectable only on the
molecular level; however, they may result in changes to the physiology or lifecycle of the

bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique
carbon source, the ability to inhabit a particular ecological niche or the ability to resist
antimicrobial agents. Different strains of E. coli are often host-specific, making it
possible to determine the source of fecal contamination in environmental samples.[citation
Depending on which E. coli strains are present in a water sample, for example,
assumptions can be made about whether the contamination originated from a human,
other mammal or bird source.
New strains of E. coli evolve through the natural biological process of mutation, and
some strains develop traits that can be harmful to a host animal. Although virulent strains
typically cause no more than a bout of diarrhea in healthy adult humans, particularly
virulent strains, such as O157:H7 or O111:B4, can cause serious illness or death in the
elderly, the very young or the immunocompromised.[4]

[edit] Biology and biochemistry

E. coli is Gram-negative, facultative anaerobic and non-sporulating. It can live on a wide
variety of substrates. E. coli uses mixed-acid fermentation in anaerobic conditions,
producing lactate, succinate, ethanol, acetate and carbon dioxide. Since many pathways
in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of
hydrogen to be low, as is the case when E. coli lives together with hydrogen-consuming
organisms such as methanogens or sulfate-reducing bacteria.[9]
Optimal growth of E. coli occurs at 37C, but some laboratory strains can multiply at
temperatures of up to 49C.[10] Growth can be driven by aerobic or anaerobic respiration,
using a large variety of redox pairs, including the oxidation of pyruvic acid, formic acid,
hydrogen and amino acids, and the reduction of substrates such as oxygen, nitrate,
dimethyl sulfoxide and trimethylamine N-oxide.[11]
Strains that possess flagella can swim and are motile, but other strains lack flagellum.
The flagella of E. coli have a peritrichous arrangement.[12]
E. coli and related bacteria possess the ability to transfer DNA via bacterial conjugation,
transduction or transformation, which allows genetic material to spread horizontally
through an existing population. It is believed that this process led to the spread of shiga
toxin from Shigella to E. coli O157:H7.[citation needed]

[edit] Normal Role

E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth,
arriving with food or water or with the individuals handling the child. In the bowel, it
adheres to the mucus of the large intestine. It is the primary facultative organism of the
human gastrointestinal tract.[13] As long as these bacteria do not acquire genetic elements
encoding for virulence factors, they remain benign commensals.[14]

[edit] Role in disease

Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal
meningitis. In rarer cases, virulent strains are also responsible for peritonitis, mastitis,
septicemia and Gram-negative pneumonia.[13] Recently it is thought that E. coli and
certain other foodborne illnesses can sometimes trigger serious health problems months
or years after patients survived that initial bout.Food poisoning can be a long-term

[edit] Virulence properties

Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence
properties.[13] Virotypes include:

Enterotoxigenic E. coli (ETEC) causative agent of diarrhea (without fever) in

humans, pigs, sheep, goats, cattle, dogs, and horses. ETEC uses fimbrial adhesins
(projections from the bacterial cell surface) to bind enterocyte cells in the small
intestine. ETEC can produce two proteinaceous enterotoxins: the larger of the two
proteins, LT enterotoxin, is similar to cholera toxin in structure and function,
while the smaller protein, ST enterotoxin causes cGMP accumulation in the
target cells and a subsequent secretion of fluid and electrolytes into the intestinal
lumen. ETEC strains are non-invasive, and they do not leave the intestinal lumen.
Enteropathogenic E. coli (EPEC) causative agent of diarrhea in humans,
rabbits, dogs, cats and horses. Like ETEC, EPEC also causes diarrhea, but the
molecular mechanisms of colonization and etiology are different. EPEC lack
fimbriae, ST and LT toxins, but they utilize an adhesin known as intimin to bind
host intestinal cells. This virotype has an array of virulence factors that are similar
to those found in Shigella, and may possess a shiga toxin. Adherence to the
intestinal mucosa causes a rearrangement of actin in the host cell, causing
significant deformation. EPEC cells are moderately-invasive (i.e. they enter host
cells) and elicit an inflammatory response. Changes in intestinal cell ultrastructure
due to "attachment and effacement" is likely the prime cause of diarrhea in those
afflicted with EPEC.
Enteroinvasive E. coli (EIEC) found only in humans. EIEC infection causes a
syndrome that is identical to Shigellosis, with profuse diarrhea and high fever.
EIEC are highly invasive, and they utilize adhesin proteins to bind to and enter
intestinal cells. They produce no toxins, but severely damage the intestinal wall
through mechanical cell destruction.
Enterohemorrhagic E. coli (EHEC) found in humans, cattle, and goats. The
sole member of this virotype is strain O157:H7, which causes bloody diarrhea and
no fever. EHEC can cause hemolytic uremic syndrome and sudden kidney failure.
It uses bacterial fimbriae for attachment, is moderately-invasive and possesses a
phage-encoded Shiga toxin that can elicit an intense inflammatory response.
Enteroaggregative E. coli (EAggEC) found only in humans. So named because
they have fimbriae which aggregate tissue culture cells, EAggEC bind to the
intestinal mucosa to cause watery diarrhea without fever. EAggEC are non-

invasive. They produce a hemolysin and an ST enterotoxin similar to that of


[edit] Gastrointestinal infection

Low-temperature electron micrograph of a cluster of E. coli bacteria, magnified 10,000

times. Each individual bacterium is oblong shaped.
Certain strains of E. coli, such as O157:H7, O121 and O104:H21, produce toxins. Food
poisoning caused by E. coli are usually associated with eating unwashed vegetables and
meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and
even life-threatening complications like Hemolytic Uremic Syndrome (HUS). This
particular strain is linked to the 2006 United States E. coli outbreak of fresh spinach.
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, contains one 'A' subunit
and five 'B' subunits arranged into one holotoxin, and is highly similar in structure and
function to Cholera toxins. The B subunits assist in adherence and entry of the toxin into
host intestinal cells, while the A subunit is cleaved and prevents cells from absorbing
water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.[15]
If E. coli bacteria escape the intestinal tract through a perforation (for example from an
ulcer, a ruptured appendix, or a surgical error) and enter the abdomen, they usually cause
peritonitis that can be fatal without prompt treatment. However, E. coli are extremely
sensitive to such antibiotics as streptomycin or gentamicin, so treatment with antibiotics
is usually effective. This could change since, as noted below, E. coli quickly acquires
drug resistance.[16]
Intestinal mucosa-associated E. coli are observed in increased numbers in the
inflammatory bowel diseases, Crohn's disease and ulcerative colitis.[17] Invasive strains of
E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the
inflamed regions correlates to the severity of the bowel inflammation.[18]
[edit] Epidemiology of gastrointestinal infection

Transmission of pathogenic E. coli often occurs via fecal-oral transmission.[19][14][20]

Common routes of transmission include: unhygienic food preparation,[19] farm
contamination due to manure fertilization,[21] irrigation of crops with contaminated
greywater or raw sewage,[22] feral pigs on cropland,[23] or direct consumption of sewagecontaminated water.[24] Dairy and beef cattle are primary reservoirs of E. coli O157:H7,[25]
and they can carry it asymptomatically and shed it in their feces.[25] Food products
associated with E. coli outbreaks include raw ground beef,[26] raw seed sprouts or spinach,
raw milk, unpasteurized juice, and foods contaminated by infected food workers via
fecal-oral route.[19]
According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission
can be disrupted by cooking food properly, preventing cross-contamination, instituting
barriers such as gloves for food workers, instituting health care policies so food industry
employees seek treatment when they are ill, pasteurization of juice or dairy products and
proper hand washing requirements.[19]
Shiga toxin-producing E. coli (STEC), specifically serotype O157:H7, have also been
transmitted by flies,[27][28][29] as well as direct contact with farm animals,[30][31] petting zoo
animals,[32] and airborne particles found in animal-rearing environments.[33]

[edit] Urinary tract infection

Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract
infections (UTI) seen in individuals with ordinary anatomy.[13] In ascending infections,
fecal bacteria colonize the urethra and spread up the urinary tract to the bladder. Because
women have a shorter urethra compared with men, they are 14-times more likely to suffer
from an ascending UTI.[13]
Uropathogenic E. coli utilize P fimbriae (pyelonephritis-associated pili) to bind urinary
tract endothelial cells and colonize the bladder. These adhesins specifically bind Dgalactose-D-galactose moieties on the P blood group antigen of erythrocytes and
uroepithelial cells.[13] Approximately 1% of the human population lacks this receptor, and
its presence or absence dictates an individual's susceptibility to E. coli urinary tract
infections. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis
of urinary tract cells.
UPEC can evade the body's innate immune defenses (e.g. the complement system) by
invading superficial umbrella cells to form intracellular bacterial communities (IBCs).[34]
They also have the ability to form K antigen, capsular polysaccharides that contribute to
biofilm formation. Biofilm-producing E. coli are recalcitrant to immune factors and
antibiotic therapy and are often responsible for chronic urinary tract infections.[35] K
antigen-producing E. coli infections are commonly found in the upper urinary tract.[13]
Descending infections, though relatively rare, occur when E. coli cells enter the upper
urinary tract organs (kidneys, bladder or ureters) from the blood stream.

[edit] Laboratory diagnosis

This section does not cite any references or sources. (December 2007)
Please improve this section by adding citations to reliable sources. Unverifiable material may be
challenged and removed.

Enteropathogenic E. coli (EPEC) and Enterotoxigenic E. coli (ETEC) - UTI or GIT

infections in infants are caused by EPEC which presents as watery diarrhea, meaning that
PMN's will not be observed in the stool neither with methylene blue nor Gram stain. First
off, G - ve, rods, with no particular arrangement are seen in Gram stain. Then, either
MacConkey agar or EMB agar (or both) are inoculated with the stool. On MacConkey
agar, deep red colonies are produced as the organism is lactose positive, and this
utilization will cause the medium's pH to drop leading to darkening of the medium.
Growth on Levine EMB agar would show black colonies with greenish-black metallic
sheen. This is diagnosic of E. coli. The organism is lysine positive, and grows on TSI
slant with a (A/A/g+/H2S-) profile. Also, IMViC is ++-- for E. coli; as it's indol positive
(red ring) and methyl red positive (bright red), but VP negative (no change-colorless) and
citrate negative (no change-green color). Serology is done using the SSS-Coagglutination
Enterohaemorrhagic E. coli O157:H7 - isolated either from urine or, more commonly,
stool. There exist three protocols for diagnosis:
(a) Diagnosis is carried out as is the case with EPEC and ETEC.
(b) Gram stain:- G - ve, rods, with no particular arrangement. Sorbitol-MacConkey agar
is a modified MacConkey agar which has sorbitol instead of lactose. EHEC would
produce colorless colonies as it can't utilize sorbitol. TSI slant and IMViC are then
performed. Serology detects O157:H7 antigens.
(c) Two bottles of verocells are used. One is inoculated with equal portions of a stool
extract and antitoxin, while the other has only a stool extract. If the first bottle shows
neutralization (no cytopathic effects) while the second doesn't, then the test is considered
positive. Otherwise, it's not. This is based on the fact that the toxin produced by this
strain is neutralized in the presence of its specific antibody, meaning that it won't be able
to exert its effects on cells.

[edit] Antibiotic therapy and resistance

Main article: Antibiotic resistance
Bacterial infections are usually treated with antibiotics. However, the antibiotic
sensitivities of different strains of E. coli vary widely. As Gram-negative organisms, E.
coli are resistant to many antibiotics that are effective against Gram-positive organisms.
Antibiotics which may be used to treat E. coli infection include amoxicillin as well as

other semi-synthetic penicillins, many cephalosporins, carbapenems, aztreonam,

trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin and the aminoglycosides.
Antibiotic resistance is a growing problem. Some of this is due to overuse of antibiotics
in humans, but some of it is probably due to the use of antibiotics as growth promoters in
food of animals.[36] A study published in the journal Science in August 2007 found that the
rate of adaptative mutations in E. coli is "on the order of 105 per genome per generation,
which is 1,000 times as high as previous estimates," a finding which may have
significance for the study and management of bacterial antibiotic resistance.[37]
Antibiotic-resistant E. coli may also pass on the genes responsible for antibiotic
resistance to other species of bacteria, such as Staphylococcus aureus. E. coli often carry
multidrug resistant plasmids and under stress readily transfer those plasmids to other
species. Indeed, E. coli is a frequent member of biofilms, where many species of bacteria
exist in close proximity to each other. This mixing of species allows E. coli strains that
are piliated to accept and transfer plasmids from and to other bacteria. Thus E. coli and
the other enterobacteria are important reservoirs of transferable antibiotic resistance.[38]

[edit] Beta-lactamase strains

Resistance to beta-lactam antibiotics has become a particular problem in recent decades,
as strains of bacteria that produce extended-spectrum beta-lactamases have become more
common.[39] These beta-lactamase enzymes make many, if not all, of the penicillins and
cephalosporins ineffective as therapy. Extended-spectrum beta-lactamaseproducing E.
coli are highly resistant to an array of antibiotics and infections by these strains is
difficult to treat. In many instances, only two oral antibiotics and a very limited group of
intravenous antibiotics remain effective.
Increased concern about the prevalence of this form of "superbug" in the United
Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with
infections and the deaths.[40] Susceptibility testing should guide treatment in all infections
in which the organism can be isolated for culture.

[edit] Phage therapy

Phage therapyviruses that specifically target pathogenic bacteriahas been developed
over the last 80 years, primarily in the former Soviet Union, where it was used to prevent
diarrhea caused by E. coli.[41] Presently, phage therapy for humans is available only at the
Phage Therapy Center in the Republic of Georgia and in Poland.[42] However, on January
2 2007, the United States FDA gave Omnilytics approval to apply its E. coli O157:H7
killing phage in a mist, spray or wash on live animals that will be slaughtered for human

[edit] Vaccination

Researchers have actively been working to develop safe, effective vaccines to lower the
worldwide incidence of E. coli infection.[44] In March of 2006, a vaccine eliciting an
immune response against the E. coli O157:H7 O-specific polysaccharide conjugated to
recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA) was reported to be
safe in children two to five years old. Previous work had already indicated that it safe for
adults.[45] A phase III clinical trial to verify the large-scale efficacy of the treatment is
In January 2007 the Canadian bio-pharmaceutical company Bioniche announced it has
developed a cattle vaccine which reduces the number of O157:H7 shed in manure by a
factor of 1000, to about 1000 pathogenic bacteria per gram of manure.[46][47][48]

[edit] Role in biotechnology

This section requires expansion.

Because of its long history of laboratory culture and ease of manipulation, E. coli also
plays an important role in modern biological engineering and industrial microbiology.[49]
The work of Stanley Norman Cohen and Herbert Boyer in E. coli, using plasmids and
restriction enzymes to create recombinant DNA, became a foundation of biotechnology.

Considered a very versatile host for the production of heterologous proteins,[51]

researchers can introduce genes into the microbes using plasmids, allowing for the mass
production of proteins in industrial fermentation processes. Genetic systems have also
been developed which allow the production of recombinant proteins using E. coli. One of
the first useful applications of recombinant DNA technology was the manipulation of E.
coli to produce human insulin.[52] Modified E. coli have been used in vaccine
development, bioremediation, and production of immobilised enzymes.[51] E. coli cannot,
however, be used to produce some of the more large, complex proteins which contain
multiple disulfide bonds and, in particular, unpaired thiols, or proteins that also require
post-translational modification for activity.[49]

[edit] Model organism

This section requires expansion.

E. coli is frequently used as a model organism in microbiology studies. Cultivated strains

(e.g. E. coli K12) are well-adapted to the laboratory environment, and, unlike wild type
strains, have lost their ability to thrive in the intestine. Many lab strains lose their ability
to form biofilms.[53][54] These features protect wild type strains from antibodies and other
chemical attacks, but require a large expenditure of energy and material resources.
In 1946, Joshua Lederberg and Edward Tatum first described the phenomenon known as
bacterial conjugation using E. coli as a model bacterium,[55] and it remains the primary

model to study conjugation.[citation needed] E. coli was an integral part of the first experiments
to understand phage genetics,[56] and early researchers, such as Seymour Benzer, used E.
coli and phage T4 to understand the topography of gene structure.[57] Prior to Benzer's
research, it was not known whether the gene was a linear structure, or if it had a
branching pattern.

[edit] See also

Bacterial water analysis

Coliform bacteria
Contamination control
Food poisoning

[edit] References
1. ^ Escherichia coli O157:H7. CDC Division of Bacterial and Mycotic Diseases. Retrieved
on 2007-01-25.
2. ^ Vogt, R.L.; L. Dippold (Mar-Apr 2005). "Escherichia coli O157:H7 outbreak
associated with consumption of ground beef, June-July 2002". Public Health Reports 2:
174-178. PMID 15842119.
3. ^ Bentley, R, Meganathan, R., Biosynthesis of Vitamin K (menaquinone) in Bacteria,
Bacteriological Reviews, 1982, 46(3):241-280. Review.
4. ^ a b Hudault, S.; J. Guignot and A.L. Servin (July 2001). "Escherichia coli strains
colonizing the gastrointestinal tract protect germfree mice against Salmonella
typhimurium infection." Gut 49:47-55. PMID 11413110.
5. ^ Reid, G.; J. Howard and B.S. Gan (September 2001). "Can bacterial interference
prevent infection?" Trends in Microbiology 9(9):424-428. PMID 11553454.
6. ^ a b Feng P, Weagant S, Grant, M (2002-09-01). Enumeration of Escherichia coli and the
Coliform Bacteria. Bacteriological Analytical Manual (8th ed.). FDA/Center for Food
Safety & Applied Nutrition. Retrieved on 2007-01-25.
7. ^ Thompson, Andrea. "E. coli Thrives in Beach Sands", Live Science, June 4, 2007.
Retrieved on 2007-12-03.
8. ^ Escherichia. Taxonomy Browser. NCBI. Retrieved on 2007-11-30.
9. ^ Madigan MT, Martinko JM (2006). Brock Biology of microorganisms, 11th ed.,
Pearson. ISBN 0-13-196893-9.
10. ^ Fotadar U, Zaveloff P, Terracio L (2005). "Growth of Escherichia coli at elevated
temperatures". J. Basic Microbiol. 45 (5): 4034. doi:10.1002/jobm.200410542. PMID
11. ^ Ingledew WJ, Poole RK (1984). "The respiratory chains of Escherichia coli".
Microbiol. Rev. 48 (3): 22271. PMID 6387427.
12. ^ Darnton NC, Turner L, Rojevsky S, Berg HC, On torque and tumbling in swimming
Escherichia coli. J Bacteriol. 2007 Mar;189(5):1756-64. Epub 2006 Dec 22.
13. ^ a b c d e f g Todar, K.. Pathogenic E. coli. Online Textbook of Bacteriology. University of
Wisconsin-Madison Department of Bacteriology. Retrieved on 2007-11-30.
14. ^ a b Evans Jr., Doyle J.; Dolores G. Evans. Escherichia Coli. Medical Microbiology, 4th
edition. The University of Texas Medical Branch at Galveston. Retrieved on 2007-12-02.

15. ^ Tauschek M, Gorrell R, Robins-Browne RM,. "Identification of a protein secretory

pathway for the secretion of heat-labile enterotoxin by an enterotoxigenic strain of
Escherichia coli". PNAS 99: 7066-7071. doi:10.1073/pnas.092152899. PMID 12011463.
16. ^ Gene Sequence Of Deadly E. Coli Reveals Surprisingly Dynamic Genome. Science
Daily (2001-01-25). Retrieved on 2007-02-08.
17. ^ Rolhion N, Darfeuille-Michaud A (2007). "Adherent-invasive Escherichia coli in
inflammatory bowel disease". Inflamm. Bowel Dis. 13 (10): 127783.
doi:10.1002/ibd.20176. PMID 17476674.
18. ^ Baumgart M, Dogan B, Rishniw M, et al (2007). "Culture independent analysis of ileal
mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny
relative to depletion of Clostridiales in Crohn's disease involving the ileum". ISME J 1
(5): 40318. doi:10.1038/ismej.2007.52. PMID 18043660.
19. ^ a b c d Retail Establishments; Annex 3 - Hazard Analysis. Managing Food Safety: A
Manual for the Voluntary Use of HACCP Principles for Operators of Food Service and
Retail Establishments. U.S. Department of Health and Human Services Food and Drug
Administration Center for Food Safety and Applied Nutrition (April 2006). Retrieved on
20. ^ Gehlbach, S.H.; J.N. MacCormack, B.M. Drake, W.V. Thompson (April 1973). "Spread
of disease by fecal-oral route in day nurseries". Health Service Reports 88 (4): 320-322.
PMID 4574421.
21. ^ a b Sabin Russell. "Spinach E. coli linked to cattle; Manure on pasture had same strain
as bacteria in outbreak", San Francisco Chronicle, Friday, October 13, 2006. Retrieved on
22. ^ Heaton, J.C.; K. Jones (October 10 2007). "Microbial contamination of fruit and
vegetables and the behaviour of enteropathogens in the phyllosphere: a review". Journal
of Applied Microbiology: 613. doi:10.1111/j.1365-2672.2007.03587.x. PMID 17927745.
23. ^ Thomas R. DeGregori (2007-08-17). CGFI: Maddening Media Misinformation on
Biotech and Industrial Agriculture. Retrieved on 2007-12-08.
24. ^ Chalmers, R.M.; H. Aird, F.J. Bolton (2000). "Waterborne Escherichia coli O157".
Society for Applied Microbiology Symposium Series (29): 124S-132S. PMID 10880187.
25. ^ a b Bach, S.J.; T.A. McAllister, D.M. Veira, V.P.J. Gannon, and R.A. Holley (2002).
"Transmission and control of Escherichia coli O157:H7". Canadian Journal of Animal
Science 82: 475490.
26. ^ Institute of Medicine of the National Academies (2002). Escherichia coli O157:H7 in
Ground Beef: Review of a Draft Risk Assessment. Washington, D.C.: The National
Academies Press. ISBN 0-309-08627-2.
27. ^ Szalanski A, Owens C, McKay T, Steelman C (2004). "Detection of Campylobacter
and Escherichia coli O157:H7 from filth flies by polymerase chain reaction". Med Vet
Entomol 18 (3): 241-6. doi:10.1111/j.0269-283X.2004.00502.x. PMID 15347391.
28. ^ Sela S, Nestel D, Pinto R, Nemny-Lavy E, Bar-Joseph M (2005). "Mediterranean fruit
fly as a potential vector of bacterial pathogens". Appl Environ Microbiol 71 (7): 4052-6.
doi:10.1128/AEM.71.7.4052-4056.2005. PMID 16000820.
29. ^ Alam M, Zurek L (2004). "Association of Escherichia coli O157:H7 with houseflies on
a cattle farm". Appl Environ Microbiol 70 (12): 7578-80. doi:10.1128/AEM.70.12.75787580.2004. PMID 15574966.
30. ^ Rahn, K.; S.A. Renwick, R.P. Johnson, J.B. Wilson, R.C. Clarke, D. Alves, S.A.
McEwen, H. Lior, J. Spika (April 1998). "Follow-up study of verocytotoxigenic
Escherichia coli infection in dairy farm families". Journal of Infectious Disease 177 (4):
1139-1140. PMID 9535003.
31. ^ Trevena, W.B.; G.A Willshaw, T. Cheasty, G. Domingue, C. Wray (December 1999).
"Transmission of Vero cytotoxin producing Escherichia coli O157 infection from farm





animals to humans in Cornwall and west Devon". Community Disease and Public Health
2 (4): 263-268. PMID 10598383.
^ Heuvelink, A.E.; C. van Heerwaarden, J.T. Zwartkruis-Nahuis, R. van Oosterom, K.
Edink, Y.T. van Duynhoven and E. de Boer (October 2002). "Escherichia coli O157
infection associated with a petting zoo". Epidemiology and Infection 129 (2): 295-302.
doi:10.1017/S095026880200732X. PMID 12403105.
^ Varma, J.K.; K.D. Greene, M.E. Reller, S.M. DeLong, J. Trottier, S.F. Nowicki, M.
DiOrio, E.M. Koch, T.L. Bannerman, S.T. York, M.A. Lambert-Fair, J.G. Wells, P.S.
Mead (November 26 2003). "An outbreak of Escherichia coli O157 infection following
exposure to a contaminated building". JAMA 290 (20): 2709-2712.
doi:10.1001/jama.290.20.2709. PMID 14645313.
^ Justice S, Hunstad D, Seed P, Hultgren S (2006). "Filamentation by Escherichia coli
subverts innate defenses during urinary tract infection". Proc Natl Acad Sci U S A 103
(52): 19884-9. doi:10.1073/pnas.0606329104. PMID 17172451.
^ Ehrlich G, Hu F, Shen K, Stoodley P, Post J (Aug 2005). "Bacterial plurality as a
general mechanism driving persistence in chronic infections". Clin Orthop Relat Res: 204. doi:10.1073/pnas.0606329104. PMID 16056021.
^ Johnson J, Kuskowski M, Menard M, Gajewski A, Xercavins M, Garau J (2006).
"Similarity between human and chicken Escherichia coli isolates in relation to
ciprofloxacin resistance status". J Infect Dis 194 (1): 71-8. doi:10.1086/504921. PMID
^ Adaptive Mutations in Bacteria: High Rate and Small Effects. Science Magazine (10
August 2007). Retrieved on 10 September, [[2007]].
^ Salyers AA, Gupta A, Wang Y (2004). "Human intestinal bacteria as reservoirs for
antibiotic resistance genes". Trends Microbiol. 12 (9): 4126.
doi:10.1016/j.tim.2004.07.004. PMID 15337162.
^ Paterson DL, Bonomo RA (2005). "Extended-spectrum beta-lactamases: a clinical
update". Clin. Microbiol. Rev. 18 (4): 65786. doi:10.1128/CMR.18.4.657-686.2005.
PMID 16223952.
^ HPA Press Statement: Infections caused by ESBL-producing E. coli.
^ Therapeutic use of bacteriophages in bacterial infections. Polish Academy of Sciences.
^ Medical conditions treated with phage therapy. Phage Therapy Center.
^ OmniLytics Announces USDA/FSIS Approval for Bacteriophage Treatment of E. coli
O157:H7 on Livestock. OmniLytics.
^ Girard M, Steele D, Chaignat C, Kieny M (2006). "A review of vaccine research and
development: human enteric infections". Vaccine 24 (15): 2732-50.
doi:10.1016/j.vaccine.2005.10.014. PMID 16483695.
^ a b Ahmed A, Li J, Shiloach Y, Robbins J, Szu S (2006). "Safety and immunogenicity of
Escherichia coli O157 O-specific polysaccharide conjugate vaccine in 2-5-year-old
children". J Infect Dis 193 (4): 515-21. doi:10.1086/499821. PMID 16425130.
^ Pearson H (2007). "The dark side of E. coli". Nature 445 (7123): 8-9.
doi:10.1038/445008a. PMID 17203031.
^ New cattle vaccine controls E. coli infections. Canada AM (2007-01-11). Retrieved on
^ Bioniche Life Sciences Inc. (2007-01-10). "Canadian Research Collaboration Produces
World's First Food Safety Vaccine: Against E. coli O157:H7". Press release. Retrieved on
^ a b Lee SY (1996). "High cell-density culture of Escherichia coli". Trends Biotechnol. 14
(3): 98105. doi:10.1016/0167-7799(96)80930-9. PMID 8867291.
^ "Special Report: The birth of biotechnology", Nature 421, 456-457 (23 January 2003)

51. ^ a b Cornelis P (2000). "Expressing genes in different Escherichia coli compartments".

Curr. Opin. Biotechnol. 11 (5): 4504. doi:10.1016/S0958-1669(00)00131-2. PMID
52. ^ Tof, Ilanit (1994). Recombinant DNA Technology in the Synthesis of Human Insulin.
Little Tree Pty. Ltd.. Retrieved on 2007-11-30.
53. ^ Fux CA, Shirtliff M, Stoodley P, Costerton JW (2005). "Can laboratory reference
strains mirror "real-world" pathogenesis?". Trends Microbiol. 13 (2): 5863.
doi:10.1016/j.tim.2004.11.001. PMID 15680764.
54. ^ Vidal O, Longin R, Prigent-Combaret C, Dorel C, Hooreman M, Lejeune P (1998).
"Isolation of an Escherichia coli K-12 mutant strain able to form biofilms on inert
surfaces: involvement of a new ompR allele that increases curli expression". J. Bacteriol.
180 (9): 24429. PMID 9573197.
55. ^ Lederberg, Joshua; E.L. Tatum (October 19 1946). "Gene recombination in E. coli".
Nature 158: 558. Source: National Library of Medicine - The Joshua Lederberg Papers
56. ^ The Phage Course - Origins. Cold Spring Harbor Laboratory (2006). Retrieved on
57. ^ Benzer, Seymour (March 1961). "On the topography of the genetic fine structure".
PNAS 47 (3): 403415. doi:10.1073/pnas.47.3.403.

[edit] External links

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[edit] General

E.coli Food poisoning can be long-term problem - Yahoo News

E. coli statistics
Spinach and E. coli Outbreak - U.S. FDA
E. coli Outbreak From Fresh Spinach - U.S. CDC
E. coli Info

[edit] Databases

EcoCyc: Encyclopedia of E. coli genes and metabolism

Uropathogenic Escherichia coli (UPEC)
NIAID Enteropathogen Resource Integration Center (ERIC) Genome information
on diarrheagenic E.coli and evolutionarily related organisms

EcoliWiki The community annotation system for E. coli K-12 and its phages and
ECODAB The structure of the O-antigens that form the basis of the serological
classification of E. coli


Major model organisms in genetics

Sheep Lambda phage E. coli Chlamydomonas Tetrahymena Budding yeast
Fission yeast Neurospora Maize Arabidopsis Medicago truncatula C. elegans
Drosophila Xenopus Zebrafish Rat Mouse
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