Enterohemorrhagic
Escherichia coli
Infections
Verocytotoxin producing
Escherichia coli (VTEC),
Shiga toxin producing
Escherichia coli (STEC),
Escherichia coli O157:H7
Last Updated: May 2009
Importance
Enterohemorrhagic Escherichia coli (EHEC) is a subset of pathogenic E. coli that
can cause diarrhea or hemorrhagic colitis in humans. Hemorrhagic colitis
occasionally progresses to hemolytic uremic syndrome (HUS), an important cause of
acute renal failure in children and morbidity and mortality in adults. In the elderly, the
case fatality rate for HUS can be as high as 50%. E. coli O157:H7 (EHEC O157:H7)
has been recognized as a cause of this syndrome since the 1980s. The reservoirs for
EHEC O157:H7 are ruminants, particularly cattle and sheep, which are infected
asymptomatically and shed the organism in feces. Other animals such as rabbits and
pigs can also carry this organism. Humans acquire EHEC O157:H7 by direct contact
with animal carriers, their feces, and contaminated soil or water, or via the ingestion
of underdone ground beef, other animal products, and contaminated vegetables and
fruit. The infectious dose is very low, which increases the risk of disease.
Infections with EHEC in other serogroups, including members of O26, O91,
O103, O104, O111, O113, O117, O118, O121, O128 and O145, are increasingly
recognized as causes of hemorrhagic colitis and HUS. Some of these organisms may
be as significant in human disease as EHEC O157:H7; however, they are not
recognized on the media used to isolate this organism, and many laboratories do not
routinely screen for other strains. Although many EHEC seem to be carried
asymptomatically in animals, members of some non-O157 serogroups may cause
enteric disease in young animals. In rabbits, EHEC O153 has been linked to a disease
that resembles HUS.
Etiology
Escherichia coli is a Gram negative rod (bacillus) in the family
Enterobacteriaceae. Most E. coli are normal commensals found in the intestinal tract.
Pathogenic strains of this organism are distinguished from normal flora by their
possession of virulence factors such as exotoxins. The specific virulence factors can
be used, together with the type of disease, to separate these organisms into
pathotypes.
Verocytotoxigenic (or verotoxigenic) E. coli (VTEC) produce a toxin that is
lethal to cultured African green monkey kidney cells (Vero cells) but not to some
other cultured cell types. There are two major families of verocytotoxins, Vt1 and
Vt2. A VTEC isolate may produce one or both toxins. Because verocytotoxin is
homologous to the shiga toxins of Shigella dysenteriae, VTEC are also called shiga
toxin-producing E. coli (STEC).
Enterohemorrhagic E. coli are VTEC that possess additional virulence factors,
giving them the ability to cause hemorrhagic colitis and hemolytic uremic syndrome
in humans. One key characteristic found in EHEC, but not exclusive to these
organisms, is the ability to cause attaching and effacing (A/E) lesions on human
intestinal epithelium. A/E lesions are characterized by close bacterial attachment to
the epithelial cell membrane and the destruction of microvilli at the site of adherence.
Some of the genes that are involved in producing A/E lesions can be used, together
with the presence of the verocytotoxin, to help identify EHEC.
Serotypes involved
E. coli are serotyped based on the O (somatic lipopolysaccharide), H (flagellar)
and K (capsular) antigens. Serotypes known to contain EHEC include E. coli
O157:H7, the non-motile organism E. coli O157:H-, and members of other
serogroups, particularly O26, O103, O111 and O145 but also O91, O104, O113,
O117, O118, O121, O128 and others. E. coli O157:H- is closely related to E. coli
O157:H7, but it not simply a nonmotile version of this organism; it also has a
distinctive combination of phenotypic and virulence features.
Serotyping alone is not enough to identify an organism as an EHEC; virulence
factors characteristic of these organisms must also be present. E. coli O157:H7 strains
are relatively homogeneous, and nearly all of these organisms carry virulence factors
associated with hemorrhagic colitis and HUS. Members of other serotypes can be
© 2009
page 1 of 10
Enterohemorrhagic Escherichia coli Infections
more heterogeneous. For example, E. coli in the serogroup
O26 may have one, both or neither verocytotoxin genes,
and only half of all E. coli O26 isolates in one study
possessed ehx, a gene found on a plasmid associated with
EHEC. Different organisms may carry distinct groups of
virulence factors. For example, the virulence gene profiles
of EHEC in serogroups O26 and O145 differ from each
other, as well as from EHEC O157:H7. Because many
virulence factors (including the verocytotoxin) are carried
on plasmids or in bacteriophages, new E. coli strains that
have novel disease patterns and/or are difficult to classify
by the current systems can emerge.
Geographic Distribution
EHEC 0157:H7 infections occur worldwide; infections
have been reported on every continent except Antarctica.
Other EHEC are probably also widely distributed. The
importance of some serotypes may vary with the
geographic area.
Transmission
EHEC are transmitted by the fecal–oral route. They can
be spread between animals by direct contact or via water
troughs, shared feed, contaminated pastures or other
environmental sources. Birds and flies are potential vectors.
In one experiment, EHEC O157:H7 was transmitted in
aerosols when the distance between pigs was at least 10
feet. The organism was thought to have become aerosolized
during high pressure washing of pens, but normal feeding
and rooting behavior may have also contributed.
The reservoir hosts and epidemiology may vary with
the organism. Ruminants, particularly cattle and sheep, are
the most important reservoir hosts for EHEC O157:H7. A
small proportion of the cattle in a herd can be responsible
for shedding more than 95% of the organisms. These
animals, which are called super-shedders, are colonized at
the terminal rectum, and can remain infected much longer
than other cattle. Super-shedders might also occur among
sheep. Animals that are not normal reservoir hosts for
EHEC O157:H7 may serve as secondary reservoirs after
contact with ruminants. EHEC O157:H7 is mainly
transmitted to humans by the consumption of contaminated
food and water, or by contact with animals, feces and
contaminated soil. Person-to-person transmission can
contribute to disease spread during outbreaks; however,
humans do not appear to be a maintenance host for this
organism. Most human cases have been linked to direct or
indirect contact with cattle, but some have been associated
with other species including sheep, goats (unpasteurized
goat milk), pigs (dry fermented pork salami), deer
(venison), horses, rabbits and birds. The infectious dose for
humans is estimated to be under 100 organisms, and might
be as few as 10.
Foodborne outbreaks with EHEC O157:H7 are often
caused by eating undercooked or unpasteurized animal
products, particularly ground beef but also other meats and
Last Updated: May 2009
© 2009
sausages, and unpasteurized milk and cheese. Other
outbreaks have been linked to alfalfa or radish sprouts,
lettuce, spinach and other contaminated vegetables, as well
as unpasteurized cider. Irrigation water contaminated with
feces is an important source of EHEC O157:H7 on
vegetables. This organism can attach to plants, and survives
well on the surface of a variety of fruits, vegetables and
fresh culinary herbs. Depending on the environmental
conditions, small numbers of bacteria left on washed
vegetables may multiply significantly over several days.
EHEC O157:H7 can be internalized in the tissues of some
plants including lettuce, where it may not be susceptible to
washing. Fruit flies can transmit this organism to apples,
where it can multiply in wounded tissues. EHEC O157:H7
can remain viable for long periods in many food products.
It can survive for at least nine months in ground beef stored
at -20°C (-4°F). It is tolerant of acidity, and remains
infectious for weeks to months in acidic foods such as
mayonnaise, sausage, apple cider and cheddar at
refrigeration temperatures. It also resists drying.
Some human cases are caused by exposure to
contaminated soil or water. EHEC are usually eliminated by
municipal water treatment, but these organisms may occur
in private water supplies such as wells. Swimming in
contaminated water, especially lakes and streams, has been
associated with some infections. Soil contamination has
caused outbreaks at campgrounds and other sites, often
when the site had been grazed earlier by livestock. The
reported survival time for EHEC O157:H7 in contaminated
soil varies from a month to more than 7 months. This
organism can also survive for 2 months or longer in some
freshwater sources, especially at cold temperatures, and it
may remain viable for two weeks in marine water. One
study indicated that EHEC O157:H7 is inactivated in slurry
within two weeks; another suggested that it can survive up
to three months.
The epidemiology of other serotypes of EHEC is
poorly understood. The reservoirs for EHEC O26 may be
animals. Members of this E. coli serogroup have been
found in various species including cattle, pigs, sheep, goats,
rabbits and chickens. They are common in healthy animals
as well as animals with diarrhea. Although the source of the
organism is not known in many human cases, some EHEC
O26 outbreaks have been foodborne (beef products and
unpasteurized milk), associated with animal contact, or
linked to water contaminated with feces. Possible personto-person transmission has also been reported. VTEC O103
has been found in cattle, sheep and goats, as well as healthy
and sick humans. In contrast, EHEC O157:H- has rarely
been isolated from cattle and horses, and it was absent in
more than 1800 fecal samples from cattle, sheep, goats and
deer in Germany and the Czech Republic. However, one
outbreak was foodborne (sausages), and contact with an
infected cow and horse were the probable sources of
infection in another outbreak. It is possible that humans are
a reservoir host for this organism.
page 2 of 10
Enterohemorrhagic Escherichia coli Infections
Disinfection
E. coli can be killed by numerous disinfectants
including 1% sodium hypochlorite, 70% ethanol, phenolic
or iodine–based disinfectants, glutaraldehyde and
formaldehyde. This organism can also be inactivated by
moist heat (121°C [250°F] for at least 15 min) or dry heat
(160–170°C [320-338°F] for at least 1 hour). Foods can be
made safe by cooking them to a minimum temperature of
160°F/ 71°C. Ionizing radiation or chemical treatment with
a sodium hypochlorite solution may reduce or eliminate
bacteria on produce.
Infections in Humans
Incubation Period
The incubation period for disease caused by EHEC
O157:H7 ranges from one to 16 days. Most infections
become apparent after 3-4 days; however, the median
incubation period was 8 days in one outbreak at an
institution.
Clinical Signs
Humans can be infected asymptomatically or they may
develop watery diarrhea, hemorrhagic colitis and/ or
hemolytic uremic syndrome. Most symptomatic cases begin
with diarrhea. Some cases resolve without treatment in
approximately a week; others progress to hemorrhagic
colitis within a few days. Hemorrhagic colitis is
characterized by diarrhea with profuse, visible blood,
accompanied by abdominal tenderness, and in many cases,
by severe abdominal cramps. Some patients have a low–
grade fever; in others, fever is absent. Nausea and vomiting
may be seen, and dehydration is possible. Many cases of
hemorrhagic colitis are self–limiting and resolve in
approximately a week. Severe colitis may result in
intestinal necrosis, perforation or the development of
colonic strictures.
Hemolytic uremic syndrome occurs in up to 16% of
patients with hemorrhagic colitis. This syndrome is most
common in children, the elderly and those who are
immunocompromised. It usually develops a week after the
diarrhea begins, when the patient is improving.
Occasionally, children develop HUS without prodromal
diarrhea. HUS is characterized by kidney failure, hemolytic
anemia and thrombocytopenia. The relative importance of
these signs varies. Some patients with HUS have hemolytic
anemia and/or thrombocytopenia with little or no renal
disease, while others have significant kidney disease but no
thrombocytopenia and/or minimal hemolysis. Extrarenal
signs including CNS involvement with lethargy, irritability
and seizures are common. In more severe cases, there may
be paresis, stroke, cerebral edema or coma. Respiratory
complications can include pleural effusion, fluid overload
and adult respiratory distress syndrome. Elevation of
pancreatic enzymes or pancreatitis may also be seen.
Last Updated: May 2009
© 2009
Rhabdomyolysis and myocardial involvement are rare. The
form of HUS usually seen in adults, particularly the elderly,
is sometimes called thrombotic thrombocytopenic purpura
(TTP). In TTP, there is typically less kidney damage than in
children, but neurologic signs including stroke, seizures and
CNS deterioration are more common. Death occurs most
often in cases with serious extrarenal disease such as severe
CNS signs. Approximately 65–85% of children recover
from HUS without permanent damage; however, long-term
renal complications including hypertension, renal
insufficiency and end-stage renal failure also occur.
Residual extrarenal problems such as transient or
permanent insulin-dependent diabetes mellitus, pancreatic
insufficiency, gastrointestinal complications or neurological
defects such as poor fine-motor coordination are possible.
Communicability
Person-to-person transmission occurs by the fecal-oral
route. Most people shed EHEC O157:H7 for approximately
7 to 9 days; a minority can excrete this organism for 3
weeks or longer after the onset of symptoms. In a few
cases, shedding may continue for several months. Young
children tend to shed the organism longer than adults.
Transmission is particularly common among children still
in diapers.
Diagnostic Tests
Because humans do not normally carry EHEC, clinical
cases can be diagnosed by finding these organisms in fecal
samples. Food and environmental samples may also be
tested to determine the source of the infection. EHEC are
sometimes difficult to identify. They are a minor population
in the fecal flora or food. They also closely resemble
commensal E. coli except in verocytotoxin production.
However, the verocytotoxin alone does not necessarily
identify an organism as EHEC; additional virulence factors
must also be present.. Many diagnostic laboratories can
detect verocytotoxin-producing E. coli (VTEC) and identify
EHEC O157:H7; non-O157 EHEC strains must often be
sent to a reference laboratory for identification. There is no
single technique that can be used to isolate all EHEC
serotypes.
Selective and differential media have been developed
for EHEC O157:H7, based on its lack of β-glucuronidase
activity and the inability of most strains to rapidly ferment
sorbitol. MacConkey agar containing 1% sorbitol (SMAC),
often with cefixime and either rhamnose or potassium
tellurite, is frequently used. Hemorrhagic colitis agar can be
used to isolate EHEC O157:H7 from foods. Other media,
including commercial chromogenic agars (e.g., rainbow
agar), are also available. Because other strains of E. coli, as
well as other bacteria, can grow on these media, prior
enrichment for E. coli O157 aids detection, particularly in
samples from food and the environment. For enrichment,
samples may be cultured in liquid enrichment medium, or
immunomagnetic separation (IMS) can be used to
page 3 of 10
Enterohemorrhagic Escherichia coli Infections
concentrate the members of serogroup O157 before plating.
In IMS, magnetic beads coated with an antibody to the
O157 antigen are used to bind these organisms.
Colonies suspected to be EHEC O157:H7 are
confirmed to be E. coli with biochemical tests, and shown
to have the O157 somatic antigen and H7 flagellar antigen
with immunoassays. A variety of tests including enzymelinked immunosorbent assays (ELISAs), agglutination,
PCR, immunoblotting or Vero cell assay can be used to
detect the verocytotoxin or its genes. Phage typing and
pulsed field gel electrophoresis can subtype EHEC
O157:H7 for epidemiology; these tests are generally done
by reference laboratories. Subtyping is important in
finding the source of an outbreak and tracing transmission.
The techniques used to identify EHEC O157:H7 can
miss atypical strains of this organism, including rare
sorbitol-fermenting isolates. They are also ineffective for
detecting EHEC O157:H–, which ferments sorbitol and is
beta-glucuronidase positive. Identification of EHEC
O157:H- is laborious, but it can be done by IMS followed
by plating samples onto SMAC and testing individual
sorbitol-fermenting colonies to detect the O157 antigen,
verocytotoxins or their genes, and/or other virulence
factors.
Selective media and isolation techniques have been
developed for few non-O157 EHEC. IMS beads are
commercially available for concentrating some common
EHEC serogroups including O26, O103, O111 and O145. A
selective rhamnose MacConkey medium containing
cefixime and tellurite (CT-RMAC) is used to isolate and
identify EHEC O26. Isolation of most non-O157 EHEC
relies on screening colonies for verocytotoxin, the genes
that produce this toxin and/or other virulence genes
associated with EHEC. MacConkey agar or other media
normally used to culture E. coli can be used to grow these
organisms. Some prescreening techniques target specific
serogroups or serotypes known to be associated with human
EHEC disease. Techniques to identify most non-O157
EHEC are very labor-intensive, and these tests are not
available at most laboratories.
Immunological and nucleic acid-based tests that detect
O and H antigens, verocytotoxin or various genes
associated with EHEC can be used for presumptive
diagnosis. These rapid tests can determine whether potential
pathogens are present in samples before isolation. They
include dipstick and membrane technologies, agglutination
tests, microplate assays, colony immunoblotting, PCR,
immunofluorescence and ELISAs. Although verocytotoxin
production can aid identification, VTEC are not necessarily
EHEC and additional virulence factors must usually be
identified. Verocytotoxin-negative derivatives of the EHEC
may occasionally be found by the time HUS develops. The
results from rapid tests are confirmed by isolating the
organism. In humans, EHEC may not be found in feces
after one week.
Last Updated: May 2009
© 2009
Serology is also valuable in humans, particularly later
in the course of the disease when EHEC are difficult to
find. Indirect ELISAs can detect antibodies to EHEC
O157:H7 for months after infection. Cross-reactions with
other bacteria can be seen.
Treatment
Treatment of hemorrhagic colitis is supportive, and
may include fluids and a bland diet. Antibiotics are
controversial and are usually avoided: they do not seem to
reduce symptoms, prevent complications or decrease
shedding, and they may increase the risk of HUS. The use
of antimotility (antidiarrheal) agents in hemorrhagic colitis
also seems to increase the risk for developing HUS. Patients
with complications may require intensive care including
dialysis, transfusion and/or platelet infusion. Patients who
develop irreversible kidney failure may need a kidney
transplant.
Prevention
Frequent hand washing, especially before eating or
preparing food, and good hygiene are important in
preventing transmission from animals and their
environment. Hand washing facilities should be available in
petting zoos and other areas where the public may contact
livestock, and eating and drinking should be discouraged at
these sites. To protect children and other household
members, people who work with animals should keep their
work clothing, including shoes, away from the main living
areas and launder these items separately. Two children
apparently became infected with EHEC O157:H7 after
contact with bird (rook) feces, possibly via their father’s
soiled work shoes or contaminated overalls. After a number
of outbreaks associated with camping in the U.K., the
Scottish E. coli O157 Task Force has recommended that
ruminants not be grazed on land for at least three weeks
before camping begins.
Techniques to reduce microbial contamination during
slaughter and meat processing can reduce the risk of EHEC
from this source. Screening and control programs have been
established for EHEC O157:H7 in meat. To prevent crosscontamination during food preparation, consumers should
wash their hands, counters, cutting boards, and utensils
thoroughly after they have been in contact with raw meat.
Meat should be cooked thoroughly to kill E. coli.
Unpasteurized milk or other dairy products and
unpasteurized juices should be avoided.
Water that may be contaminated should not be used to
irrigate vegetable crops, and untreated manure/ effluents
should not be used on fruits or vegetables that will be eaten
raw. Post-harvest measures include thorough washing of
vegetables under running water to reduce bacterial
numbers. Vegetables can also be disinfected with a dilute
chlorine solution. It is safest to wash vegetables
immediately before use; under some environmental
conditions, populations of bacteria can build up again after
page 4 of 10
Enterohemorrhagic Escherichia coli Infections
a few days. EHEC carried internally in plant tissues are
difficult to destroy except by irradiation or cooking.
Contamination of public water supplies is prevented by
standard water treatment procedures. Livestock-should be
kept away from private water supplies. Microbiological
testing can also be considered. To the extent possible,
people should avoid swallowing water when swimming or
playing in lakes, ponds and streams.
Good hygiene, careful hand-washing and proper
disposal of infectious feces can reduce person-to-person
transmission. Thorough hand washing is especially
important after changing diapers, after using the toilet, and
before eating or preparing food. Bed linens, towels and
soiled clothing from patients with hemorrhagic colitis
should be washed separately, and toilet seats and flush
handles should be cleaned appropriately. In some areas,
regulations may prohibit infected children from attending
daycare or school until they are no longer shedding
organisms. Some authors suggest that isolating infected
children from their young siblings or other young
household members can significantly decrease the risk of
secondary spread.
The risk to humans can also be reduced if EHEC
carriage is decreased or eliminated in animals (see below).
Morbidity and Mortality
EHEC infections can occur as sporadic cases or in
outbreaks. In North America, EHEC O157:H7 infections
are most common from summer to autumn. In the U.K, they
tend to occur from late spring to late summer. Seasonality
might be caused by seasonal shedding patterns in animals,
or it could be due to other factors such as eating
undercooked meat at summer barbecues. In contrast, EHEC
O157:H- infections, which are most common in children
under 3 years of age, tend to be seen in the winter.
The incidence of EHEC in humans is difficult to
determine, because cases of uncomplicated diarrhea may
not be tested for these organisms. In 2004, the estimated
annual incidence of EHEC O157:H7 reported in Scotland,
the U.S., Germany, Australia, Japan and the Republic of
Korea ranged from 0.08 to 4.1 per 100,000 population, with
the highest incidence in Scotland. In the U.S., the Centers
for Disease Control and Prevention (CDC) estimates that
EHEC O157:H7 causes approximately 73,000 illnesses,
2,000 hospitalizations, and 50-60 deaths each year. The
prevalence of non-O157 EHEC in human disease is
probably underestimated, because most laboratories do not
routinely screen for these organisms. In the U.S., the CDC
estimates that the incidence of non-O157 EHEC is probably
similar to O157 EHEC. In continental Europe, Latin
America and Australia, some evidence suggests than nonO157 EHEC infections may be more common in humans
than EHEC O157:H7.
In clinical cases, the mortality rate varies with the
syndrome. Hemorrhagic colitis alone is usually self–
Last Updated: May 2009
© 2009
limiting, but death is possible. The number of cases that
progress to HUS varies with the organism and the
outbreak. Approximately 5-10% of patients with
hemorrhagic colitis from EHEC O157:H7 usually develop
HUS; however, a 16% incidence was reported during a
particularly virulent outbreak associated with spinach in
the U.S. Complications and fatalities are particularly
common among children, the elderly, and those who are
immunosuppressed or have debilitating illnesses. HUS is
fatal in 3–10% of children and TTP in up to 50% of the
elderly.
Infections in Animals
Species Affected
Ruminants, especially cattle and sheep, are the major
reservoirs for EHEC 0157:H7. Bison and deer can be
infected. This organism can sometimes be found in other
mammals including pigs, rabbits, horses, dogs, raccoons
and opossums, and in birds including chickens, turkeys,
geese, pigeons, gulls, rooks and various other wild birds.
In some instances, it is not known whether a species
normally serves as a reservoir host or if it is only a
temporary carrier. For example, rabbits shedding EHEC
O157:H7 have caused outbreaks in humans, but most
infected rabbits have been found near farms with infected
cattle.
The reservoir hosts for non-O157 EHEC are poorly
understood. Members of serogroup O26 have been found in
cattle, pigs, sheep, goats, rabbits and chickens; however, all
of these organisms are not necessarily EHEC. VTEC O103
has been found in cattle, sheep and goats, as well as healthy
and sick humans. EHEC O145 can occur in cattle, but less
often than EHEC O26. One serotype, EHEC O145:H-, was
isolated from a cat associated with a human case; whether
the child infected the cat or the cat infected the child was
uncertain. EHEC O157:H- has been found in a cow and a
horse, but surveys in Germany and the Czech Republic
suggest that this serotype is generally rare or absent in
cattle, sheep, goats and deer. Domesticated rabbits appear
to be reservoir hosts for EHEC O153:H- and O153:H7.
Clinical Signs
EHEC O157:H7 has not been associated with illness in
naturally infected animals. In experimentally infected
calves, this serotype does not seem to cause disease in
animals older than one week of age. There is one report of
bloody or mucoid diarrhea, with some deaths, after
experimental infection of neonatal (less than 2-day-old)
calves. Another study reported illness in gnotobiotic piglets.
Dogs that were experimentally inoculated with EHEC
O157:H7 developed transient acute diarrhea with decreased
appetite and vomiting, but recovered spontaneously without
complications in 1-2 days. In the same experiment, dogs
inoculated with a non-O157 EHEC developed severe
disease, with diarrhea and vomiting followed by lethargy
page 5 of 10
Enterohemorrhagic Escherichia coli Infections
and inappetence, dehydration and dramatic weight loss.
These dogs also had neurological signs including seizures,
cerebral infarction, blindness and coma, and died 5-6 days
after the onset of clinical signs.
Members of some non-O157 EHEC serogroups
including O26, O111, O118 and O103 may cause diarrhea
and other gastrointestinal signs in young animals. EHEC
O118:H16 is often associated with diarrhea in calves, and
this has been confirmed by experimental challenge in
newborn calves. However, epidemiological studies for most
EHEC are suggestive rather than definitive. There are
relatively few studies in animals using defined strains of E.
coli, and most of these experiments were done before
EHEC virulence determinants were well understood. VTEC
strains that have been associated with diarrhea in
experimentally infected calves include VTEC O5:H-,
VTEC O8:H9, VTEC O26:H11, VTEC O26:H-, VTEC
O26, VTEC O80:H- and VTEC O111:H-. In many but not
all cases, the diarrhea was bloody and mucoid.
EHEC O153:H- has been linked to an outbreak of
hemorrhagic diarrhea and an illness that resembled HUS in
domesticated rabbits. Experimentally infected rabbits
developed hemorrhagic diarrhea with lethargy, inappetence,
dehydration and weight loss.
Communicability
Subclinically infected animals can shed EHEC.
Shedding may be transient or intermittent, and animals that
have stopped excreting this organism can be recolonized.
Calves are more likely to shed EHEC O157:H7 than adult
cattle. Experimentally infected pigs could shed this
organism for at least 2 months.
Post Mortem Lesions
Click to view images
EHEC lesions in ruminants are usually characterized
by inflammation of the intestinal mucosa, and are generally
limited to the large intestine. In some cases, a
fibrinohemorrhagic exudate is present.
In rabbits experimentally infected with EHEC O153,
the cecum and/or proximal colon were edematous and
thickened, and the serosal surfaces had petechial or
ecchymotic hemorrhages. Pale kidneys were also reported.
Dogs infected with EHEC O157:H7 had no significant
gross lesions. In dogs inoculated with a non-O157 EHEC
strain, the primary cause of death was microvascular
thrombosis leading to kidney failure and multiple organ
failure. This syndrome resembled HUS. In these dogs,
inflammation and edema occurred in the small and large
intestines. The kidneys were pale, with a few petechiae on
the serosal surface. The liver was enlarged, with
inflammation and necrotic lesions.
Diagnostic Tests
EHEC are zoonotic and the infectious dose is low.
Caution should be used when handling samples;
laboratory infections have been reported.
Last Updated: May 2009
© 2009
Carrier animals are usually detected by finding EHEC
in fecal samples, which are either freshly voided or taken
directly from the animal. Rectoanal swabs may also be used
in some cases. Intestinal contents can be collected at
slaughter. Repeated sampling, as well as sampling more
animals, increases the chance of detection. In some studies,
samples have been collected from hides in addition to feces.
One study suggested that the EHEC O157H7 status for a
cattle farm or pen could be determined by walking around
the pen in a pair of disposable, liquid absorbing overshoes.
Samples should be kept cool (4°C/ 39°F) and cultured as
soon as possible.
EHEC can be difficult to identify. They are a minor
population in the fecal flora of animals. They also closely
resemble commensal E. coli except in verocytotoxin
production. However, the verocytotoxin alone does not
necessarily identify an organism as EHEC; additional
virulence factors must also be present. Many diagnostic
laboratories can detect verocytotoxin-producing E. coli
(VTEC) and identify EHEC O157:H7; non-O157 EHEC
strains must often be sent to a reference laboratory for
identification. There is no single technique that can be used
to isolate all EHEC serotypes.
Selective and differential media have been developed
for EHEC O157:H7, based on its lack of β-glucuronidase
activity and the inability of most strains to rapidly ferment
sorbitol. MacConkey agar containing 1% sorbitol (SMAC),
often with cefixime and either rhamnose or potassium
tellurite, is frequently used. Hemorrhagic colitis agar can be
used to isolate EHEC O157:H7 from foods. Other media,
including commercial chromogenic agars (e.g., rainbow
agar), are also available. Because other strains of E. coli, as
well as other bacteria, can grow on these media, prior
enrichment for E. coli O157 aids detection. For enrichment,
samples may be cultured in liquid enrichment medium, or
immunomagnetic separation (IMS) can be used to
concentrate the members of serogroup O157 before plating.
In IMS, magnetic beads coated with an antibody to the
O157 antigen are used to bind these organisms.
Colonies suspected to be EHEC O157:H7 are
confirmed to be E. coli with biochemical tests, and shown
to have the O157 somatic antigen and H7 flagellar antigen
with immunoassays. A variety of tests including enzymelinked immunosorbent assays, agglutination, PCR,
immunoblotting or Vero cell assay can be used to detect the
verocytotoxin or its genes. Phage typing and pulsed field
gel electrophoresis can subtype EHEC O157:H7 for
epidemiology; these tests are generally done by reference
laboratories.
The techniques used to identify EHEC O157:H7 can
miss atypical strains of this organism, including rare
sorbitol-fermenting isolates. They are also ineffective for
detecting EHEC O157:H–, which ferments sorbitol and is
beta-glucuronidase positive. Identification of EHEC
O157:H- is laborious, but can be done by IMS followed by
page 6 of 10
Enterohemorrhagic Escherichia coli Infections
plating samples onto SMAC and testing individual sorbitolfermenting colonies to detect the O157 antigen,
verocytotoxins, and/or other virulence factors.
Selective media and isolation techniques have been
developed for few non-O157 EHEC. IMS beads are
commercially available for concentrating some common
EHEC serogroups including O26, O103, O111 and O145. A
selective rhamnose MacConkey medium containing
cefixime and tellurite (CT-RMAC) is used to isolate and
identify EHEC O26. Isolation of most non-O157 EHEC
relies on screening colonies for verocytotoxin, the genes
that produce this toxin and/or other virulence genes
associated with EHEC. MacConkey agar or other media
normally used to culture E. coli can be used to grow these
organisms. Some prescreening techniques target specific
serogroups or serotypes known to be associated with human
EHEC disease. Techniques to identify most non-O157
EHEC are very labor-intensive, and these tests are not
available at most laboratories.
Immunological and nucleic acid-based tests that detect
O and H antigens, verocytotoxin or various genes
associated with EHEC can be used for presumptive
diagnosis. These rapid tests can determine whether potential
pathogens are present in samples before isolation. They
include dipstick and membrane technologies, agglutination
tests, microplate assays, colony immunoblotting, PCR,
immunofluorescence and ELISAs. Although verocytotoxin
production can aid identification, VTEC are common in
animals, and these organisms are not necessarily EHEC;
additional virulence factors must also be identified.
Verocytotoxin-negative derivatives of EHEC can occur.
The results from rapid tests are confirmed by isolating the
organism. Some kits validated for food and meat samples
and kits for human clinical samples may lack sensitivity
when testing fecal samples from animals.
Although cattle can produce antibodies to O157,
serology is not used routinely in animals to diagnose
infections with VTEC or EHEC.
Prevention
Prevention of shedding in domesticated animals,
particularly ruminants, is expected to decrease the number
of human infections. These techniques are still in
development. Identifying and targeting super-shedders
should be particularly effective. The removal of supershedders from the herd might be helpful. In one study,
allowing a pasture to lie fallow for the winter prevented the
transmission of EHEC O157:H7 to susceptible animals the
following spring. Other proposed interventions include
vaccination; the application of disinfectants (e.g.,
chlorhexidine), various antimicrobial chemicals or
bacteriophages to the terminal rectum; and the use of
probiotics that would preferentially colonize the
gastrointestinal tract. Dietary manipulations have also been
proposed. These interventions are still in the research stage.
Last Updated: May 2009
© 2009
Management practices to decrease EHEC in the
environment include the storage of effluents on a cement
floor for 3 months or longer before discharge, and the
collection of all liquids in a trap to minimize leaching of
liquid manure into groundwater. Some EHEC may remain
after long-term storage, and untreated manure and effluents
should not be used on fruit and vegetable crops that will be
eaten raw. To prevent transmission to animals, they should
not be allowed to graze pastures for a period after effluent
has been applied. Composting or treatment of manure
before use as a fertilizer may reduce the risks from this
source. During composting, the survival of the organism
varies with the size of the compost heap, the temperature
attained, and the dose of the organism. Other biological
processes (aerobic and anaerobic digestion), heat drying,
and/or chemical treatments have been proposed to sanitize
farm effluents before discharge into the environment; the
effect of some chemical treatments on the environment has
not yet been determined.
Methods to eliminate EHEC from infected companion
animals have not been established. However, oral
autovaccination with a heat-inactivated EHEC strain (
O145:H–) stopped shedding of the organism in a
persistently infected cat.
Morbidity and Mortality
Surveys suggest that EHEC O157:H7 is widespread in
cattle herds, but the prevalence in individual animals is low.
Some studies have found that this organism is more
common in cattle during the summer and early autumn. One
study reported that the prevalence was higher when it was
cooler, but more bacteria were shed in the summer. Other
studies have not found seasonal patterns of shedding.
Prevalence rates for EHEC O157:H7 among cattle vary
from less than 1% to 36%, depending on the country, type
of herd studied and other conditions. One study suggested
that 28% of the cattle at U.S. slaughterhouses carried EHEC
O157:H7 during the summer. In a recent survey, 97% of
U.S. agricultural fairs had at least one animal infected with
EHEC O157:H7. Overall, this organism was isolated from
11.4% of the cattle, 1.2% of the pigs, 3.6% of the sheep and
goats, and 5.2% of the fly pools at these fairs. In the U.K.,
estimates of the prevalence of EHEC O157:H7 in sheep
range from 2.2 to 7.4%. In one study, the transient
prevalence of this organism in sheep was 31%. A recent
study from the U.S. found that many bison also carry EHEC
O157:H7: the overall prevalence was 47%, and fecal
prevalence on different sampling days varied from 17% to
83%. The prevalence in deer is reported to be less than 3%,
and some surveys estimate that it is less than 0.5%.
Sampling of wild rabbits associated with infected cattle
farms found that 9.5% to 40% of the rabbits also carried
this organism. One study reported that 2% of swine colon
samples collected at slaughter contained EHEC O157:H7.
Recent studies that use sensitive methods for detection
report a higher prevalence than early surveys. However,
page 7 of 10
Enterohemorrhagic Escherichia coli Infections
highly sensitive techniques may also overestimate
prevalence, as some animals shedding the organism may
not be colonized, but only transiently infected by
transmission from super-shedders or the environment.
Little is known about the prevalence of most non-O157
EHEC. One study reported that the mean prevalence for
VTEC (not EHEC) was 31% in cattle and 42% in sheep.
However, a gene associated with EHEC (eaeA) was more
likely to be found in cattle VTEC isolates (16.5%) than
sheep VTEC (7.5%).
Potential EHEC seem to be uncommon in most nonruminant species. The prevalence of VTEC in dogs, cats,
chickens and pigs appears to be much lower than in
ruminants. EHEC O153 may be relatively common in
rabbits. In one study, 25% of Dutch belted rabbits and 9%
of the New Zealand white rabbits from one commercial
source had EHEC O153:H- or O153:H7 in their feces.
Morbidity in adult ruminants appears to be negligible
or absent. Young animals may be affected by some
serogroups of EHEC. Deaths have been reported in some
experimentally infected animals including some calves,
dogs inoculated with a non-O157 EHEC, and rabbits
inoculated with EHEC O153. The morbidity and mortality
rates are currently unknown.
Internet Resources
Centers for Disease Control and Prevention (CDC)
http://www.cdc.gov/nczved/dfbmd/disease_listing/stec_gi.html
Medical Microbiology
http://www.ncbi.nlm.nih.gov/books/NBK7627/
MicroBioNet. Serotypes of VTEC
www.microbionet.com.au/VTECtable.htm
Public Health Agency of Canada. Material Safety Data
Sheets
http://www.phac-aspc.gc.ca/msds-ftss/index-eng.php
The Institute of Food Technologists
http://www.ift.org
The Merck Manual of Diagnosis and Therapy
http://www.merck.com/pubs/mmanual/
U.S. FDA Foodborne Pathogenic Microorganisms and
Natural Toxins Handbook (Bad Bug Book)
http://vm.cfsan.fda.gov/~mow/intro.html
USDA. FSIS. E coli 0157:H7
http://www.fsis.usda.gov/factsheets/E_coli/index.asp
World Organization for Animal Health (OIE)
http://www.oie.int
OIE Manual of Diagnostic Tests and Vaccines for
Terrestrial Animals
http://www.oie.int/international-standardsetting/terrestrial-manual/access-online/
Last Updated: May 2009
© 2009
OIE Terrestrial Animal Health Code
http://www.oie.int/international-standardsetting/terrestrial-code/access-online/
References
Alam MJ, Zurek L. Seasonal prevalence of Escherichia coli
O157:H7 in beef cattle feces. J Food Prot. 2006;69(12):3018-20.
Animal Health Australia. The National Animal Health Information
System [NAHIS] E. coli 0111, 0157 [online]. Available at:
http://www.brs.gov.au/usr–bin/aphb/ahsq?dislist=alpha.*
Accessed 8 Oct 2002.
Ateba CN, Bezuidenhout CC. Characterisation of Escherichia coli
O157 strains from humans, cattle and pigs in the North-West
Province, South Africa. Int J Food Microbiol.
2008;128(2):181-8.
Avery LM, Williams AP, Killham K, Jones DL.Survival of
Escherichia coli O157:H7 in waters from lakes, rivers,
puddles and animal-drinking troughs. Sci Total Environ.
2008;389(2-3):378-85.
Bielaszewska M, Köck R, Friedrich AW, von Eiff C,
Zimmerhackl LB, Karch H, Mellmann A. Shiga toxinmediated hemolytic uremic syndrome: time to change the
diagnostic paradigm? PLoS ONE. 2007;2(10):e1024.
Buchanan RL, Doyle MP. Foodborne disease significance of
Escherichia coli 0157:H7 and other enterohemorrhagic E coli.
Food Technol. 1997;51(10): 69–76.
Busch U, Hörmansdorfer S, Schranner S, Huber I, Bogner KH,
Sing A. Enterohemorrhagic Escherichia coli excretion by
child and her cat. Emerg Infect Dis. 2007;13(2):348-9.
Centers for Disease Control and Prevention [CDC]. Division of
Foodborne, Bacterial and Mycotic Diseases [DFBMD].
Escherichia coli [online]. CDC DFBMD; 2008 Mar. Available
at:
http://www.cdc.gov/nczved/dfbmd/disease_listing/stec_gi.html.
Accessed 3 Mar 2009.
Chalmers RM, Salmon RL, Willshaw GA, Cheasty T, Looker N,
Davies I, Wray C. Vero-cytotoxin-producing Escherichia coli
O157 in a farmer handling horses. Lancet.
1997;349(9068):1816.
Chase-Topping M, Gally D, Low C, Matthews L, Woolhouse M.
Super-shedding and the link between human infection and
livestock carriage of Escherichia coli O157. Nat Rev
Microbiol. 2008;6(12):904-12.
Cobbaut K, Houf K, Douidah L, Van Hende J, De Zutter L.
Alternative sampling to establish the Escherichia coli O157
status on beef cattle farms. Vet Microbiol. 2008;132(1-2):
205-10.
Cornick NA, Vukhac H. Indirect transmission of Escherichia coli
O157:H7 occurs readily among swine but not among sheep.
Appl Environ Microbiol. 2008;74(8):2488-91.
DebRoy C, Roberts E. Screening petting zoo animals for the
presence of potentially pathogenic Escherichia coli. J Vet
Diagn Invest. 2006;18(6):597-600.
Dipineto L, Santaniello A, Fontanella M, Lagos K, Fioretti A,
Menna LF. Presence of Shiga toxin-producing Escherichia
coli O157:H7 in living layer hens. Lett Appl Microbiol.
2006;43(3):293-5.
page 8 of 10
Enterohemorrhagic Escherichia coli Infections
Dunn JR, Keen JE, Moreland D, Alex T. Prevalence of
Escherichia coli O157:H7 in white-tailed deer from Louisiana.
J Wildl Dis. 2004;40(2):361-5.
Ejidokun OO, Walsh A, Barnett J, Hope Y, Ellis S, Sharp MW,
Paiba GA, Logan M, Willshaw GA, Cheasty T. Human Vero
cytotoxigenic Escherichia coli (VTEC) O157 infection linked
to birds. Epidemiol Infect. 2006;134(2):421-3.
Fenwick B. E. coli O157 food poisoning/HUS in dogs [online].
1996. Available at: http://hayato.med.osaka–u.ac.jp/o–157–
HUS.html.* Accessed 12 Nov 2002.
Fremaux B, Prigent-Combaret C, Vernozy-Rozand C. Long-term
survival of Shiga toxin-producing Escherichia coli in cattle
effluents and environment: an updated review. Vet Microbiol.
2008;132(1-2):1-18.
Foster G, Evans J, Knight HI, Smith AW, Gunn GJ, Allison LJ,
Synge BA, Pennycott. Analysis of feces samples collected
from a wild-bird garden feeding station in Scotland for the
presence of verocytotoxin-producing Escherichia coli O157.
Appl Environ Microbiol. 2006;72(3):2265-7.
Garcia A, Bosques CJ, Wishnok JS, Feng Y, Karalius BJ,
Butterton JR, Schauer DB, Rogers AB, Fox JG. Renal injury
is a consistent finding in Dutch Belted rabbits experimentally
infected with enterohemorrhagic Escherichia coli. J Infect Dis.
2006;193(8):1125-34.
García A, Fox JG. The rabbit as a new reservoir host of
enterohemorrhagic Escherichia coli. Emerg Infect Dis.
2003;9(12):1592-7.
García-Sánchez A, Sánchez S, Rubio R, Pereira G, Alonso JM,
Hermoso de Mendoza J, Rey J. Presence of Shiga toxinproducing E. coli O157:H7 in a survey of wild artiodactyls.
Vet Microbiol. 2007;121(3-4):373-7.
Guentzel, MN. Escherichia, Klebsiella, Enterobacter, Serratia,
Citrobacter and Proteus. In: Baron S, editor. Medical
microbiology. 4th ed. New York: Churchill Livingstone; 1996.
Available at:
http://www.gsbs.utmb.edu/microbook/ch026.htm. Accessed
12 Nov 2002.
Jenkins C, Evans J, Chart H, Willshaw GA, Frankel G.
Escherichia coli serogroup O26--a new look at an old
adversary. J Appl Microbiol. 2008;104(1):14-25.
Karama M, Johnson RP, Holtslander R, Gyles CL. Phenotypic and
genotypic characterization of verotoxin-producing Escherichia
coli O103:H2 isolates from cattle and humans. J Clin
Microbiol. 2008;46(11):3569-75.
Karch H, Tarr PI, Bielaszewska M. Enterohaemorrhagic
Escherichia coli in human medicine. Int J Med Microbiol.
2005;295(6-7):405-18.
Keen JE, Wittum TE, Dunn JR, Bono JL, Durso LM. Shigatoxigenic Escherichia coli O157 in agricultural fair livestock,
United States. Emerg Infect Dis. 2006;12(5):780-6.
Lee JH, Hur J, Stein BD.Occurrence and characteristics of
enterohemorrhagic Escherichia coli O26 and O111 in calves
associated with diarrhea. Vet J. 2008;176(2):205-9.
Leomil L, Pestana de Castro AF, Krause G, Schmidt H, Beutin L.
Characterization of two major groups of diarrheagenic
Escherichia coli O26 strains which are globally spread in
human patients and domestic animals of different species.
FEMS Microbiol Lett. 2005;249(2):335-42.
Last Updated: May 2009
© 2009
Low JC, McKendrick IJ, McKechnie C, Fenlon D, Naylor SW,
Currie C, Smith DG, Allison L, Gally DL. Rectal carriage of
enterohemorrhagic Escherichia coli O157 in slaughtered
cattle. Appl Environ Microbiol. 2005;71(1):93-7.
Matthews L, Low JC, Gally DL, Pearce MC, Mellor DJ,
Heesterbeek JA, Chase-Topping M, Naylor SW, Shaw DJ,
Reid SW, Gunn GJ, Woolhouse ME. Heterogeneous shedding
of Escherichia coli O157 in cattle and its implications for
control. Proc Natl Acad Sci U S A. 2006;103(3):547-52.
Naylor SW, Gally DL, Low JC. Enterohaemorrhagic E. coli in
veterinary medicine. Int J Med Microbiol. 2005;295(6-7):419-41.
Naylor SW, Nart P, Sales J, Flockhart A, Gally DL, Low JC.
Impact of the direct application of therapeutic agents to the
terminal recta of experimentally colonized calves on
Escherichia coli O157:H7 shedding. Appl Environ Microbiol.
2007;73(5):1493-500.
Porter RS, Kaplan JL, Homeier BP, Beers MH, editors. The
Merck manual of diagnosis and therapy [online]. 18th ed.
Whitehouse Station, NJ: Merck and Co.;2005. Escherichia
coli infections. Available at:
http://www.merck.com/mmpe/sec14/ch173/ch173f.html#sec1
4-ch173-ch173f-720. Accessed 3 Mar 2009.
Public Health Agency of Canada. Material Safety Data Sheet –
Escherichia coli, enterohemorrhagic. Office of Laboratory
Security; 2001 Jan. Available at: http://www.phacaspc.gc.ca/msds-ftss/msds63e-eng.php. Accessed 2 Mar 2009.
Rasmussen MA, Casey TA.Environmental and food safety aspects
of Escherichia coli O157:H7 infections in cattle. Crit Rev
Microbiol. 2001;27(2):57-73.
Reinstein S, Fox JT, Shi X, Alam MJ, Nagaraja TG. Prevalence of
Escherichia coli O157:H7 in the American bison (Bison
bison). J Food Prot. 2007;70(11):2555-60.
Renter DG, Sargeant JM. Enterohemorrhagic Escherichia coli
O157: epidemiology and ecology in bovine production
environments. Anim Health Res Rev. 2002;3(2):83-94.
Sargeant JM, Amezcua MR, Rajic A, Waddell L. Pre-harvest
interventions to reduce the shedding of E. coli O157 in the
faeces of weaned domestic ruminants: a systematic review.
Zoonoses Public Health. 2007;54(6-7):260-77.
Sass DA, Chopra KB, Regueiro MD. Pancreatitis and E. coli
O157:H7 colitis without hemolytic uremic syndrome. Dig Dis
Sci. 2003;48(2):415-6.
Scaife HR, Cowan D, Finney J, Kinghorn-Perry SF, Crook B.
Wild rabbits (Oryctolagus cuniculus) as potential carriers of
verocytotoxin-producing Escherichia coli. Vet Rec.
2006;159(6):175-8.
Scheiring J, Andreoli SP, Zimmerhackl LB. Treatment and outcome
of Shiga-toxin-associated hemolytic uremic syndrome (HUS).
Pediatr Nephrol. 2008;23(10):1749-60.
Schouten JM, Graat EA, Frankena K, VAN Zijderveld F, DE Jong
MC. Transmission and quantification of verocytotoxinproducing Escherichia coli O157 in dairy cattle and calves.
Epidemiol Infect. 2009;137(1):114-23.
Seto EY, Soller JA, Colford JM Jr. Strategies to reduce person-toperson transmission during widespread Escherichia coli
O157:H7 outbreak. Emerg Infect Dis. 2007;13(6):860-6.
page 9 of 10
Enterohemorrhagic Escherichia coli Infections
Silvestro L, Caputo M, Blancato S, Decastelli L, Fioravanti A,
Tozzoli R, Morabito S, Caprioli A. Asymptomatic carriage of
verocytotoxin-producing Escherichia coli O157 in farm workers
in Northern Italy. Epidemiol Infect. 2004;132(5):915-9.
Sonntag AK, Zenner E, Karch H, Bielaszewska M. Pigeons as a
possible reservoir of Shiga toxin 2f-producing Escherichia
coli pathogenic to humans. Berl Munch Tierarztl Wochenschr.
2005;118(11-12):464-70.
Stephens TP, Loneragan GH, Thompson TW, Sridhara A,
Branham LA, Pitchiah S, Brashears MM. Distribution of
Escherichia coli 0157 and Salmonella on hide surfaces, the
oral cavity, and in feces of feedlot cattle. J Food Prot.
2007;70(6):1346-9.
Stordeur P, China B, Charlier G, Roels S, Mainil J. Clinical signs,
reproduction of attaching/effacing lesions, and enterocyte
invasion after oral inoculation of an O118 enterohaemorrhagic
Escherichia coli in neonatal calves. Microbes Infect.
2000;2(1):17-24.
Strachan NJ, Dunn GM, Locking ME, Reid TM, Ogden ID.
Escherichia coli O157: burger bug or environmental
pathogen? Int J Food Microbiol. 2006;112(2):129-37.
Ulinski T, Lervat C, Ranchin B, Gillet Y, Floret D, Cochat P.
Neonatal hemolytic uremic syndrome after mother-to-child
transmission of Escherichia coli O157. Pediatr Nephrol.
2005;20(9):1334-5.
Walderhaug M. Escherichia coli O157:H7. In: U.S. Food & Drug
Administration [(FDA], Center for Food Safety & Applied
Nutrition [CFSAN] ,Foodborne pathogenic microorganisms and
natural toxins handbook [online]. FDA CFSAN;2001 Jan.
Available at: http://www.cfsan.fda.gov/
~mow/chap15.html. Accessed 3 Mar 2009.
Wang JY, Wang SS, Yin PZ. Haemolytic-uraemic syndrome
caused by a non-O157 : H7 Escherichia coli strain in
experimentally inoculated dogs. J Med Microbiol. 2006;55
(Pt 1):23-9.
Welinder-Olsson C, Kaijser B. Enterohemorrhagic Escherichia
coli (EHEC). Scand J Infect Dis. 2005;37(6-7):405-16.
Werber D, Mason BW, Evans MR, Salmon RL. Preventing
household transmission of Shiga toxin-producing Escherichia
coli O157 infection: promptly separating siblings might be the
key. Clin Infect Dis. 2008;46(8):1189-96.
Whitworth JH, Fegan N, Keller J, Gobius KS, Bono JL, Call DR,
Hancock DD, Besser TE. International comparison of clinical,
bovine, and environmental Escherichia coli O157 isolates on
the basis of Shiga toxin-encoding bacteriophage insertion site
genotypes. Appl Environ Microbiol. 2008;74(23):7447-50.
Williams AP, McGregor KA, Killham K, Jones DL.Persistence
and metabolic activity of Escherichia coli O157:H7 in farm
animal faeces.FEMS Microbiol Lett. 2008;287(2):168-73.
World Organization for Animal Health [OIE]. Manual of
diagnostic tests and vaccines for terrestrial animals [online].
Paris: OIE; 2008. Verocytotoxigenic Escherichia coli.
Available at:
http://www.oie.int/eng/normes/mmanual/2008/pdf/2.09.11_V
ERO_E_COLI.pdf. Accessed 1 Mar 2009.
Yoon JW, Hovde CJ. All blood, no stool: enterohemorrhagic
Escherichia coli O157:H7 infection. J Vet Sci. 2008;9(3):
219-31.
Last Updated: May 2009
© 2009
Zweifel C, Schumacher S, Beutin L, Blanco J, Stephan
R.Virulence profiles of Shiga toxin 2e-producing Escherichia
coli isolated from healthy pig at slaughter. Vet Microbiol.
2006;117(2-4):328-32.
*Link defunct as of 2009
page 10 of 10