Bacillus coli communis Escherich 1885
Escherichia coli (/ˌɛʃəˈrɪkiə ˈkoʊlɪ/
/ˌɛʃəˈrɪkiə ˈkoʊlaɪ/; commonly abbreviated E. coli) is a
gram-negative, rod-shaped bacterium that is commonly found in the
lower intestine of warm-blooded organisms (endotherms). Most E. coli
strains are harmless, but some serotypes are pathogenic and can cause
serious food poisoning in humans, and are occasionally responsible for
E. coli are also responsible for a majority of
cases of urinary tract infections. The harmless strains are part of
the normal flora of the gut, and can benefit their hosts by producing
vitamin K2, and by preventing the establishment of pathogenic
bacteria within the intestine.
2.1 O antigen
2.2 K antigen
2.3 H antigen
3 Role in disease
3.1 Gastrointestinal infection
3.1.1 Virulence properties
3.1.2 Epidemiology of gastrointestinal infection
Urinary tract infection
Neonatal meningitis (NMEC)
3.4 Possible role in colorectal cancer
3.5 Animal diseases
4 Laboratory diagnosis
Antibiotic therapy and resistance
6 Phage therapy
8 See also
E. coli and related bacteria constitute about 0.1% of gut flora,
and fecal–oral transmission is the major route through which
pathogenic strains of the bacterium cause disease. Cells are able to
survive outside the body for a limited amount of time, which makes
them ideal indicator organisms to test environmental samples for fecal
contamination. The bacterium can also be grown easily and
inexpensively in a laboratory setting, and has been intensively
investigated for over 60 years.
E. coli is the most widely studied
prokaryotic model organism, and an important species in the fields of
biotechnology and microbiology, where it has served as the host
organism for the majority of work with recombinant DNA.
German paediatrician and bacteriologist
Theodor Escherich discovered
E. coli in 1885, and it is now classified as part of the
Enterobacteriaceae family of gamma-proteobacteria.
Structure of a lipopolysaccharide
E. coli strains can be categorized based on elements that
can elicit an immune response in animals, namely:
O antigen: part of lipopolysaccharide layer
K antigen: capsule
H antigen: flagellin
E. coli strain EDL933 is of the O157:H7 group.
Main article: O antigen
The outer membrane of an
E. coli cell contains millions of
lipopolysaccharide (LPS) molecules, which consists of:
O antigen, a polymer of immunogenic repeating oligosaccharides (1–40
Core region of phosphorylated nonrepeating oligosaccharides
Lipid A (endotoxin)
O antigen is used for serotyping
E. coli and these O group
designations go from O1 to O181, with the exception of some groups
which have been historically removed, namely O31, O47, O67, O72, O93
(now K84), O94, and O122; groups 174 to 181 are provisional (O174=OX3
and O175=OX7) or are under investigation (176 to 181 are
STEC/VTEC). Additionally subtypes exist for many O groups (e.g.
O128ab and O128ac). It should be noted though that antibodies
towards several O antigens cross-react with other O antigens and
partially to K antigens not only from E. coli, but also from other
Escherichia species and
O antigen is encoded by the rfb gene cluster. rol (cld) gene
encodes the regulator of lipopolysaccharide O-chain length.
See also: Polysaccharide § Bacterial capsular polysaccharides
The acidic capsular polysaccharide (CPS) is a thick, mucous-like,
layer of polysaccharide that surrounds some pathogen E. coli.
There are two separate groups of K-antigen groups, named group I and
group II (while a small in-between subset (K3, K10, and K54/K96) has
been classified as group III). The former (I) consist of 100 kDa
(large) capsular polysaccharides, while the latter (II), associated
with extraintestinal diseases, are under 50 kDa in size.
Group I K antigens are only found with certain O-antigens (O8, O9,
O20, and O101 groups), they are further subdivided on the basis of
absence (IA, similar to that of Klebsiella species in structure) or
presence (IB) of amino sugars and some group I K-antigens are attached
to the lipid A-core of the lipopolysaccharide (KLPS), in a similar way
to O antigens (and being structurally identical to O antigens in some
instances are only considered as K antigens when co-expressed with
another authentic O antigen).
Group II K antigens closely resemble those in gram-positive bacteria
and greatly differ in composition and are further subdivided according
to their acidic components, generally 20–50% of the CPS chains are
bound to phospholipids.
In total there are 60 different K antigens that have been recognized
(K1, K2a/ac, K3, K4, K5, K6, K7 (=K56), K8, K9 (=O104), K10, K11, K12
(K82), K13(=K20 and =K23), K14, K15, K16, K18a, K18ab (=K22), K19,K24,
K26, K27, K28, K29, K30, K31, K34, K37, K39, K40, K41,K42, K43, K44,
K45, K46, K47, K49 (O46), K50, K51, K52, K53, K54 (=K96), K55, K74,
K84, K85ab/ac (=O141), K87 (=O32), K92, K93, K95, K97, K98, K100,
K101, K102, K103, KX104, KX105,and KX106).
See also: flagella
The H antigen is a major component of flagella, involved in E. coli
movement. It is generally encoded by the fliC gene.
There are 53 identified H antigens, numbered from H1 to H56 (H13 and
H22 were not
E. coli antigens but from Citrobacter freundii, and H50
was found to be the same as H10).
Role in disease
In humans and in domestic animals, virulent strains of
E. coli can
cause various diseases.
In humans : gastroenteritis, urinary tract infections, and
neonatal meningitis. In rarer cases, virulent strains are also
responsible for hemolytic-uremic syndrome, peritonitis, mastitis,
septicaemia and gram-negative pneumonia.
Low-temperature electron micrograph of a cluster of
E. coli bacteria,
magnified 10,000 times. Each individual bacterium is a rounded
Certain strains of E. coli, such as O157:H7, O104:H4, O121, O26, O103,
O111, O145, and O104:H21, produce potentially lethal toxins. Food
poisoning caused by
E. coli can result from eating unwashed vegetables
or poorly butchered and undercooked meat. O157:H7 is also notorious
for causing serious and even life-threatening complications such as
hemolytic-uremic syndrome. This particular strain is linked to the
2006 United States E. coli outbreak due to fresh spinach. The O104:H4
strain is equally virulent.
Antibiotic and supportive treatment
protocols for it are not as well-developed (it has the ability to be
very enterohemorrhagic like O157:H7, causing bloody diarrhea, but also
is more enteroaggregative, meaning it adheres well and clumps to
intestinal membranes). It is the strain behind the deadly June 2011 E.
coli outbreak in Europe. Severity of the illness varies considerably;
it can be fatal, particularly to young children, the elderly or the
immunocompromised, but is more often mild. Earlier, poor hygienic
methods of preparing meat in Scotland killed seven people in 1996 due
E. coli poisoning, and left hundreds more infected.
E. coli can
harbour both heat-stable and heat-labile enterotoxins. The latter,
termed LT, contain one A subunit and five B subunits arranged into one
holotoxin, and are 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.
E. coli bacteria escape the intestinal tract through a perforation
(for example from an ulcer, a ruptured appendix, or due to 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. Recent
research suggests treatment of enteropathogenic
E. coli with
antibiotics may not improve the outcome of the disease,[citation
needed] as it may significantly increase the chance of developing
E. coli are observed in increased numbers
in the inflammatory bowel diseases,
Crohn's disease and ulcerative
colitis. 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.
Gastrointestinal infections can cause the body to develop memory T
cells to attack gut microbes that are in the intestinal tract.Food
poisoning can trigger an immune response to microbial gut bacteria.
Some researchers suggest that it can lead to inflammatory bowel
E. coli (EC) are classified on the basis of serological
characteristics and virulence properties. The major pathotypes of
E. coli that cause diarrhea are listed below.
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.
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 noninvasive, and they do not leave the intestinal
lumen. ETEC is the leading bacterial cause of diarrhea in children in
the developing world, as well as the most common cause of traveler's
diarrhea. Each year, ETEC causes more than 200 million cases of
diarrhea and 380,000 deaths, mostly in children in developing
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 aetiology are different. EPEC lack ST and LT toxins,
but they use an adhesin known as intimin to bind host intestinal
cells. This pathotype has an array of virulence factors that are
similar to those found in Shigella. 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.
E. coli (EIEC)
found only in humans
EIEC infection causes a syndrome that is identical to shigellosis,
with profuse diarrhea and high fever.
E. coli (EHEC)
found in humans, cattle, and goats
The most infamous member of this pathotype 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
E. coli common pilus, ECP), is moderately invasive and
possesses a phage-encoded shiga toxin that can elicit an intense
E. coli (EAEC)
found only in humans
So named because they have fimbriae which aggregate tissue culture
cells, EAEC bind to the intestinal mucosa to cause watery diarrhea
without fever. EAEC are noninvasive. They produce a hemolysin and an
ST enterotoxin similar to that of ETEC.
E. coli (AIEC)
found in humans
AIEC are able to invade intestinal epithelial cells and replicate
intracellularly. It is likely that AIEC are able to proliferate more
effectively in hosts with defective innate immunity. They are
associated with the ileal mucosa in Crohn's disease.
Epidemiology of gastrointestinal infection
Transmission of pathogenic
E. coli often occurs via fecal–oral
transmission. Common routes of transmission include:
unhygienic food preparation, farm contamination due to manure
fertilization, irrigation of crops with contaminated greywater or
raw sewage, feral pigs on cropland, or direct consumption of
sewage-contaminated water. Dairy and beef cattle are primary
E. coli O157:H7, and they can carry it
asymptomatically and shed it in their feces. Food products
E. coli outbreaks include cucumber, raw ground
beef, raw seed sprouts or spinach, raw milk, unpasteurized
juice, unpasteurized cheese and foods contaminated by infected food
workers via fecal–oral route.
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.
E. coli (STEC), specifically serotype O157:H7,
have also been transmitted by flies, as well as direct
contact with farm animals, petting zoo animals, and
airborne particles found in animal-rearing environments.
Urinary tract infection
E. coli bacteria
E. coli (UPEC) is responsible for approximately 90% of
urinary tract infections (UTI) seen in individuals with ordinary
anatomy. In ascending infections, fecal bacteria colonize the
urethra and spread up the urinary tract to the bladder as well as to
the kidneys (causing pyelonephritis), or the prostate in males.
Because women have a shorter urethra than men, they are 14 times more
likely to suffer from an ascending UTI.
E. coli use P fimbriae (pyelonephritis-associated pili)
to bind urinary tract urothelial cells and colonize the bladder. These
adhesins specifically bind D-galactose-D-galactose moieties on the P
blood-group antigen of erythrocytes and uroepithelial cells.
Approximately 1% of the human population lacks this receptor,[citation
needed] and its presence or absence dictates an individual's
susceptibility or non-susceptibility, respectively, to
E. coli urinary
tract infections. Uropathogenic
E. coli produce alpha- and
beta-hemolysins, which cause lysis of urinary tract cells.
Another virulence factor commonly present in UPEC is the Dr family of
adhesins, which are particularly associated with cystitis and
pregnancy-associated pyelonephritis. The Dr adhesins bind Dr blood
group antigen (Dra) which is present on decay accelerating factor
(DAF) on erythrocytes and other cell types. There, the Dr adhesins
induce the development of long cellular extensions that wrap around
the bacteria, accompanied by the activation of several signal
transduction cascades, including activation of PI-3 kinase.
UPEC can evade the body's innate immune defences (e.g. the complement
system) by invading superficial umbrella cells to form intracellular
bacterial communities (IBCs). They also have the ability to form K
antigen, capsular polysaccharides that contribute to biofilm
E. coli are recalcitrant to immune
factors and antibiotic therapy, and are often responsible for chronic
urinary tract infections. K antigen-producing
E. coli infections
are commonly found in the upper urinary tract.
Descending infections, though relatively rare, occur when E. coli
cells enter the upper urinary tract organs (kidneys, bladder or
ureters) from the blood stream.
Neonatal meningitis (NMEC)
It is produced by a serotype of
Escherichia coli that contains a
capsular antigen called K1. The colonization of the newborn's
intestines with these strains, that are present in the mother's
vagina, lead to bacteremia, which leads to meningitis. And because
of the absence of the
IgM antibodies from the mother (these do not
cross the placenta because
FcRn only mediates the transfer of IgG),
plus the fact that the body recognizes as self the K1 antigen, as it
resembles the cerebral glycopeptides, this leads to a severe
meningitis in the neonates.
Possible role in colorectal cancer
E. coli strains contain a polyketide synthase genomic island
(pks), which encodes a multi-enzymatic machinery that produces
colibactin, a substance that damages DNA. About 20% of humans are
E. coli that harbor the pks island. Colibactin can
cause cellular senescence or cancer by damaging DNA. However,
the mucosal barrier prevents
E. coli from reaching the surface of
Mucin production diminishes in the presence of
inflammation. Only when some inflammatory condition co-occurs with
E. coli infection the bacterium is able to deliver colibactin to
enterocytes and induce tumorogenesis.
In animals, virulent strains of
E. coli are responsible of a variety
of diseases, among others septicemia and diarrhea in newborn calves,
acute mastitis in dairy cows, colibacillosis also associated with
chronic respiratory disease with Mycoplasma where it causes
perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in
Alabama rot in dogs.
Most of the serotypes isolated from poultry are pathogenic only for
birds. So avian sources of
E. coli do not seem to be important sources
of infections in other animals.
Colibacillosis in domestic chicken
Mastitis in cows
In stool samples, microscopy will show gram-negative rods, with no
particular cell arrangement. 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
fermentation of this sugar will cause the medium's pH to drop, leading
to darkening of the medium. Growth on EMB agar produces black colonies
with a greenish-black metallic sheen. This is diagnostic of E. coli.
The organism is also lysine positive, and grows on
TSI slant with a
(A/A/g+/H2S-) profile. Also,
IMViC is + + – - for E. coli; as it
is indole-positive (red ring) and methyl red-positive (bright red),
but VP-negative (no change-colourless) and citrate-negative (no
change-green colour). Tests for toxin production can use mammalian
cells in tissue culture, which are rapidly killed by shiga toxin.
Although sensitive and very specific, this method is slow and
Typically, diagnosis has been done by culturing on sorbitol-MacConkey
medium and then using typing antiserum. However, current latex assays
and some typing antisera have shown cross reactions with non-E. coli
O157 colonies. Furthermore, not all
O157 strains associated
with HUS are nonsorbitol fermentors.
The Council of State and Territorial Epidemiologists recommend that
clinical laboratories screen at least all bloody stools for this
pathogen. The U.S. Centers for Disease Control and Prevention
recommend that "all stools submitted for routine testing from patients
with acute community-acquired diarrhea (regardless of patient age,
season of the year, or presence or absence of blood in the stool) be
simultaneously cultured for
E. coli O157:H7 (
O157 STEC) and tested
with an assay that detects Shiga toxins to detect non-O157
Antibiotic therapy and 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 semisynthetic 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 animal feeds. A
study published in the journal Science in August 2007 found the rate
of adaptative mutations in
E. coli is "on the order of 10−5 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.
E. coli may also pass on the genes responsible
for antibiotic resistance to other species of bacteria, such as
Staphylococcus aureus, through a process called horizontal gene
E. coli bacteria often carry multiple drug resistance
plasmids, and under stress, readily transfer those plasmids to other
species. Mixing of species in the intestines allows
E. coli to accept
and transfer plasmids from and to other bacteria. Thus,
E. coli and
the other enterobacteria are important reservoirs of transferable
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. These
beta-lactamase enzymes make many, if not all, of the penicillins and
cephalosporins ineffective as therapy. Extended-spectrum
E. coli (ESBL E. coli) are highly resistant
to an array of antibiotics, and infections by these strains are
difficult to treat. In many instances, only two oral antibiotics and a
very limited group of intravenous antibiotics remain effective. In
2009, a gene called
New Delhi metallo-beta-lactamase
New Delhi metallo-beta-lactamase (shortened NDM-1)
that even gives resistance to intravenous antibiotic carbapenem, were
E. coli bacteria.
Increased concern about the prevalence of this form of "superbug" in
United Kingdom has led to calls for further monitoring and a
UK-wide strategy to deal with infections and the deaths.
Susceptibility testing should guide treatment in all infections in
which the organism can be isolated for culture.
Phage therapy—viruses that specifically target pathogenic
bacteria—has been developed over the last 80 years, primarily in the
former Soviet Union, where it was used to prevent diarrhea caused by
E. coli. Presently, phage therapy for humans is available only at
the Phage Therapy Center in the Republic of Georgia and in Poland.
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
consumption. The enterobacteria phage T4, a highly studied phage,
E. coli for infection.
Researchers have actively been working to develop safe, effective
vaccines to lower the worldwide incidence of
E. coli infection. In
March 2006, a vaccine eliciting an immune response against the E. coli
O157:H7 O-specific polysaccharide conjugated to recombinant exotoxin A
Pseudomonas aeruginosa (O157-rEPA) was reported to be safe in
children two to five years old. Previous work had already indicated it
was safe for adults. A phase III clinical trial to verify the
large-scale efficacy of the treatment is planned.
In 2006, Fort Dodge Animal Health (Wyeth) introduced an effective,
live, attenuated vaccine to control airsacculitis and peritonitis in
chickens. The vaccine is a genetically modified avirulent vaccine that
has demonstrated protection against O78 and untypeable strains.
In January 2007, the Canadian biopharmaceutical 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.
In April 2009, a Michigan State University researcher announced he had
developed a working vaccine for a strain of E. coli. Dr. Mahdi Saeed,
Professor of epidemiology and infectious disease in MSU's colleges of
Veterinary Medicine and
Human Medicine, has applied for a patent for
his discovery and has made contact with pharmaceutical companies for
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1993 Jack in the Box
2005 South Wales (O157)
2006 North American (spinach; O157:H7)
2006 North American (multiple; O157:H7)
2009 United Kingdom
2011 Germany (O104:H4)
2015 United States
Long-term evolution experiment
T4 rII system
Bacterial disease: Proteobacterial G−
primarily A00–A79, 001–041, 080–109
Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus
Rocky Mountain spotted fever
Japanese spotted fever
North Asian tick typhus
Queensland tick typhus
Flinders Island spotted fever
African tick bite fever
American tick bite fever
Rickettsia aeschlimannii infection
Flea-borne spotted fever
Ehrlichiosis: Anaplasma phagocytophilum
Human granulocytic anaplasmosis, Anaplasmosis
Human monocytotropic ehrlichiosis
Ehrlichiosis ewingii infection
Bartonellosis: Bartonella henselae
Either B. henselae or B. quintana
Carrion's disease, Verruga peruana
Meningococcal disease, Waterhouse–Friderichsen syndrome,
Eikenella corrodens/Kingella kingae
Burkholderia cepacia complex
Bordetella pertussis/Bordetella parapertussis
Rhinoscleroma, Klebsiella pneumonia
Escherichia coli: Enterotoxigenic
Enterobacter aerogenes/Enterobacter cloacae
Citrobacter koseri/Citrobacter freundii
Typhoid fever, Paratyphoid fever, Salmonellosis
Shigellosis, Bacillary dysentery
Proteus mirabilis/Proteus vulgaris
Far East scarlet-like fever
Brazilian purpuric fever
Legionella pneumophila/Legionella longbeachae
Aeromonas hydrophila/Aeromonas veronii
Campylobacteriosis, Guillain–Barré syndrome
Peptic ulcer, MALT lymphoma, Gastric cancer