Escherichia coli

In 1989, EPA claimed E. coli is a Primary Pathogen in Sludge Biosolids that only causes Gastroenteritis

It is claimed E. coli may have been a benign bacteria in earlier times when scientists didn't play at being God. However,
in those earlier times it wasn't called E. coli. It was called Bacillus coli communis  and it could be just as deadly  Later it
was discovered that E. coli DNA could be manipulated to produce drugs, pesticides, fuel, etc.

After 12 brain surgeries, UK boy recovers from battle with E. coli
Ben Chapman
With two boys under four, I get pretty emotional when I read a story about a child getting sick from food borne illness.
This week Jack had a cold, and I felt helpless when he said "make me feel better." I can't imagine what Thomas Miller's
parents felt like over the past two years as they saw him battling the effects of E. coli infection complications which
included a septicemia and rare brain impacts. Thomas' illness was linked to eating contaminated burgers and is being
reported as the first time an individual in the UK has recovered from these complications. The youngster, who was two-
years-old at the time, fell ill just 24 hours after eating a beef burger on a family day out in Scotland in 2009.
His older brother James, then seven, suffered diarrhoeaand a day later Thomas started to pass blood.
‘We just didn’t know what was happening. It was frightening,’ said 37-year-old Mrs Miller, from Aspatria,Cumbria. ‘He
went for an operation that day and had to have dialysis. ‘He was holding his head and screaming, he couldn’t move and
was as stiff as a board.’ The E.coli had entered Thomas’ bloodstream but further scans revealed it was also attacking
his brain. Two golf ball-sized abscesses on his brain, which had caused him to go blind, were drained in August 2009 –
allowing him to see again. But his ordeal wasn’t over as he developed more abscesses on the brain and even suffered
an allergic reaction to the medication, which ‘burned’ his skin. Finally last year, after having all the abscesses removed,
he was given the all clear. ‘I’ll never forget the day he came out of intensive care,’ said Mrs Miller. ‘It’s only really this
year that I’ve been able to relax.’

EPA's scientists seems to have missed the fact that even the least virulent E. coli can be a killer. Outside
the stomach and colon, the endogenous coliform E. coli, with no virulence factors, have been
implicated in respiratory tract infections such as pneumonia, blood poisoning (septicaemia), endotoxic
shock, high blood pressure, scarring and eventually kidney failure, mental changes or confusion,
neonatal meningitis, and urinary tract infections leading to serious infections of the prostate
(prostatitis), bladder, and kidneys (pyelonephiritis) and death. According to Palomar College
Microbiology Instructor, Ana Dowey, “50 to 80% of urinary tract infections in healthy people are
produced by self-contamination from endogenous strains of E. coli.” E. coli, with no virulence factors.
This is called an opportunistic pathogen. That also means 20 to 50% of the urinary tract infections
could be from taking a bath in E. coli contaminated tap water.

In 1900, Glasgow physician Edward McCharg reported fifty-seven genital infections
during childbirth. Thirty one infections caused by streptococcus and bacillus coli were fatal.

Before E. coli took on Theodor Escherich's name, it was one of the first documented bacterial killers.
By 1903, Scientists like William Savage MD were well aware that there were varying virulence levels
between members of Bacillus coli (B. coli). However, he was of the opinion that only exposure to B.
coli from humans was of concern in drinking water. His wish was to have a test that separated human
B. coli from environmental strains of similar coli forms of bacteria.

In 1904, Christiaan Eijkman discovered some strains of E. coli could grow above 112.1°F. He claimed
the higher temperature differentiated them from environmental strains which scientists agreed had no
sanitary significance. This strain of thermotolerant E. coli assumed the name fecal coliform. E. coli
strains that grew at optimum growth temperature of 98.6°F were named coliform by the Public Health
Service in 1914 and also considered to have no sanitary significance. It is amazing that after one
hundred and seven years some scientists still believe the myth. Yet, the medical profession has always
had a different view of what was then called Coli bacillus or Bacillus coli and tested it at normal body

In the 1910 article, “Discussion On Infections Of The Urinary Tract By Bacillus Coli In Infancy And
Childhood,” Charles R. Box, et al., reported the progression of the infections in infants and young
children, including death.

In the 1919 edition of “Modern Surgery” John Chalmers Da Costa, stated, “This bacillus may be
responsible for appendicitis, peritonitis [thin tissue that lines the inner wall of the abdomen and covers
most of the abdominal organs], inflammation of the genito-urinary tract, pneumonia, inflammation of
the intestine, leptomeningitis [form of meningitis which complicates the course of all of the acute
infections], perineal abscess [between vaginal opening and rectum], cholangitis [infection of the
common bile duct], cholecystitis [bacterial infection superimposed on an obstruction of the biliary
tree], myelitis [inflammation of the spinal cord], puerperal fever [bacterial infection contracted by
women during childbirth or miscarriage], wound infections and septicemia [bacteria contaminating the
blood]. It is the cause of many abscesses about the intestine and responsible for many ischiorectal
abscesses [region between the rectum and ishial tuberosity – sitz bone].”

In the 1921 study “
” according to Leonard S. Dudgeon,
“A great point has been made by those who believe that all urinary infections are primarily via the
blood stream in that the B. coli can be obtained in pure culture from the blood, but the fact that such
bacilli may be so recovered does not point to the origin of the infection, since in view of Thiele and
Embleton's experiments, even if the colon bacillus did start from the urethral mucous membrane it
would still be found in the blood. A careful examination of the blood in B. coli infections of the urinary
tract has shown that such bacilli may be isolated very frequently, especially if the blood is taken at the
height of the rigor. Cabot and Crabtree (1916) obtained positive blood cultures in 40 percent of cases
out of 32 examined. Conclusion:
(1) Bactllus coli in infected urine can be divided into two groups: (i) haemolytic; (ii) non-haemolytic.
(2) The haemolytic group is the common type in the infection in men and the non-haemolytic in

In the 1984 New England Journal of Medicine article “
Mortality Associated with Nosocomial Urinary-
Tract Infection
,” R. Platt and associates reported that hospital acquired UTIs were deadly. They stated,
“Seventy-six patients (25 infected and 51 noninfected) died during hospitalization; death rates were 19
per cent in infected patients and 4 per cent in noninfected patients”

Urinary tract infections often occur from fecal material getting into the urethra. In 1934 study, Edith E.
Nicholls reported on “
.” Hemolytic
means the bacteria break down red blood cells. She found that in appropriate doses, both types of
bacteria killed white mice. Greater numbers of hemolyic bacteria were more likely to be found in
people with "diarrhea or colitis." However, time and temperature could cause the bacteria to lose the
hemolytic capability. According to Nicholls, "Fifty to one hundred per cent of the specimens, from each
individual, showed hemolytic Bacillus coli." The specific finding was, "The hemolytic strains of
Bacillus coli recovered from stool specimens were found to be only slightly more virulent for white
mice than were the nonhemolytic."

According to EPA, “2% to 7% of children and elderly infected with E. coli [0157;H7], may develop
hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail; 33% of
persons with hemolytic uremic syndrome have abnormal kidney function many years later, and a few
require long-term dialysis, a smaller percentage of persons with hemolytic uremic syndrome develop
high blood pressure, seizures, blindness, paralysis, and the effects of having part of their bowel
In a 1935 study, “A Study of B. coli mutabile from an Outbreak of Diarrhea in the New-born,” Anna
Dean Dulaney, Ph.D., and I. D. Michelson, M.D. of the Medical School at the University of Tennessee,
Memphis, reported the first outbreak of B. coli diarrhea among new-born infants in the Memphis
General Hospital during the winter of 1933-34. The mortality rate was 47%.

Todar's Online Textbook of Bacteriology states, “It was not until 1935 that a strain of E. coli was
shown to be the cause of an outbreak of diarrhea among infants. The GI tract of most warm-blooded
animals is colonized by E. coli within hours or a few days after birth. The bacterium is ingested in
foods or water or obtained directly from other individuals handling the infant. The human bowel is
usually colonized within 40 hours of birth. E. coli can adhere to the mucus overlying the large intestine.
Once established, an E. coli strain may persist for months or years. Resident strains shift over a long
period (weeks to months), and more rapidly after enteric infection or antimicrobial chemotherapy that
perturbs the normal flora. The basis for these shifts and the ecology of Escherichia coli in the intestine
of humans are poorly understood despite the vast amount of information on almost every other aspect
of the organism's existence.”

Today, there are more than 200 hydrogen sulfide producing variants of E. coli and an unknown number
of pathogenic chimeric clones including 3,520 unique strains of E. coli 0157:H7 reported to CDC
PulseNet between 1996 and 2006.

The “E. coli Reference Center (formerly Gastroenteric Disease Center) is a part of Animal Diagnostic
Laboratory in the Department of Veterinary and Biomedical Sciences” at PennState houses “the largest
repository for E. coli strains in America. It holds more than 70,000 strains collected over the last 50
years from animals, humans, birds and environment.”
Since the mid-1970s E.coli has been the work-horse of the genetic engineering researchers. It has
accepted genes inserted in the laboratory from other bacteria, viruses, yeast, plants and humans,
including antibiotic resistant marker genes. Since that time it has become infamous for containing the
Shiga-toxin genes such as stx1, stx2, rfb and EHEC hlyA (shiga-toxigenic Escherichia coli (STEC))
which causes bloody diarrhoea, haemorrhagic colitis (HC) and haemolytic uraemic syndrome (HUS).
The use of antibiotics on STEC may cause an immediate release of deadly toxins, and shortly
thereafter, death.

In 1989, EPA claimed pathogenic strains of E. coli in “treated” sludge (biosolids) only caused
gastroenteritis (diarrhea associated with nausea and vomiting). Even that small warning was removed
from the final regulation. According to the International Escherichia and Klebsiella Centre (WHO), it
has a very large strain collection of approximately 60,000 E. coli strains, most of which are clinical
isolates. This collection includes test and reference strains for O, K, H and F antigens, various toxins
and other E. coli virulence factors. The collection contains strains representing almost any possible
sero- and virulence type.

2010, Morbidity and Mortality Weekly Report (MMWR), “Detection of Enterobacteriaceae Isolates
Carrying Metallo-Beta-Lactamase --- United States, 2010,” CDC reported, “During January--June
2010, three Enterobacteriaceae isolates carrying a newly described resistance mechanism, the New
Delhi metallo-beta-lactamase (NDM-1) (1), were identified from three U.S. states at the CDC
antimicrobial susceptibility laboratory. This is the first report of NDM-1 in the United States, and the
first report of metallo-beta-lactamase carriage among Enterobacteriaceae in the United States. These
isolates, which include an Escherichia coli, Klebsiella pneumoniae, and Enterobacter cloacae, carry
blaNDM-1, which confers resistance to all beta-lactam agents except aztreonam (a monobactam
antimicrobial) (1); all three isolates were aztreonam resistant, presumably by a different mechanism. In
the United Kingdom, where these organisms are increasingly common, carriage of Enterobacteriaceae
containing blaNDM-1 has been closely linked to receipt of medical care in India and Pakistan (2). All
three U.S. isolates were from patients who received recent medical care in India.”

E. coli in Animals

E. coli causes colibacillosis in animals. According to the Merk vetmanual, “Colibacillosis occurs as an
acute fatal septicemia or subacute pericarditis and airsacculitis. It is a common systemic disease of
economic importance in poultry and is seen worldwide.”

Baby Calf Health: Common Diarrheal Diseases
Colibacillosis usually occurs in calves 1-10 days old. “E. coli organisms are part of the normal flora of
the intestinal tract. Many strains are harmless to the calf, but certain strains can cause moderate to
severe scours and even death. E. coli typically produces a secretory diarrhea resulting from the
intestinal epithelial cells being switched from an absorption mode to a secretion mode. E. coli is often
referred to as "white" scours and is the most common cause of calf scours.
3 Types
Enteric. This is the most common type. The main clinical sign is severe diarrhea. The calf rapidly
becomes weak and dehydrated with an initial fever that rapidly returns to normal (or subnormal).
Dehydration can lead to death.
Enterotoxigenic. (K-99 strain) This infection runs a rapid, fatal course. Toxins cause so much fluid to
be pumped into the intestine that the calf usually dies before external signs of diarrhea are present. This
type of scours is one of the few that occur within the first 3 days of life.
Septicemic. This type acts like Salmonella by invading the blood stream and penetrating body tissues
causing a general infection. Gross lesions are usually minimal. This is a rapid form of E. coli, often
with no evidence of diarrhea. Colostrum deprived calves usually die of this form of E. coli.

As far back as 1891, bacteria was found to cause illness in cows. In the 1891 article,
said, “In the Agricultural Year-Book of Switzerland for 1888, Professor Hess, of Berne, published the
results of an inquiry into the causes of mastitis in cows. He proved that the infectious forms of mastitis
are due to several and distinct kinds of bacteria, which penetrate through the milk canals into the milk
glands. Within the latter they find a soil suitable for their growth, and for the development of their
specific pathogenic properties. The resulting inflammation of the tissues is at times so mild, and the
alterations in the secretion so slight, that the affected cows can still be milked, and the milk used for
domestic purposes or for the manufacture of cheese. The milk from one affected cow, by being mixed
with milk from healthy cows, can infect large quantities with the active bacteria. The determination of
the nature and the action of these bacteria is, therefore, of hygienic and economic importance.

In the 2003 study, “
S everity of E. coli mastitis is mainly determined by cow factors ,” Christian
Burvenich, et al., Ghent University at Merelbeke, Belgium, reported, “Escherichia coli causes
inflammation of the mammary gland in dairy cows around parturition and during early lactation with
striking local and sometimes severe systemic clinical symptoms. This disease affects many high
producing cows in dairy herds and may cause several cases of death per year in the most severe cases.
It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis
susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli
mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli
mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we
know that the neutrophil is a key factor in the cows' defense against intramammary infection with E.
coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection
and the outcome of E. coli mastitis.”

In the 2009 study, “
Human Health Hazards from Antimicrobial-Resistant Escherichia coli of Animal
,” Anette M. Hammerum, et al., National Center for Antimicrobials and Infection Control,
Statens Serum Institut at Copenhagen, reported, “E. coli is a commensal bacterium in the intestine of
poultry, cattle, and pigs that are used for food production, and food of animal origin can be
contaminated with E. coli during slaughter of the animals. E. coli from meat has mostly been associated
with intestinal pathogenic E. coli (e.g., enteropathogenic, enterotoxigenic, and verotoxigenic E. coli),
but recently, E. coli of animal origin has been shown to also be associated with extra-intestinal
infections, such as urinary tract infections. In humans, the majority of infections caused by E. coli are
not harmful (e.g., uncomplicated urinary tract infections), whereas other infections (e.g., blood stream
infections) may be lethal. In many cases, the origin of E. coli that cause infection in humans remains
unknown, and the significance of the animal reservoir of antimicrobial-resistant E. coli has not been

In the 2011 Virginia Cooperative Extension bulletin, “
Escherichia coli: A Practical Summary for
Controlling Mastitis,
” Christina S. Petersson-Wolfe, Assistant Professor, Dairy Science, Virginia Tech,
and John Currin, Assistant Professor, Virginia-Maryland Regional College of Veterinary Medicine,
reported, "... the control of environmental pathogens still remains a daunting task. Escherichia coli are
Gram-negative bacteria, similar in structure to Klebsiella spp. E. coli mastitis is typically associated
with a quick onset and often severe clinical signs. -- These organisms are commonly found in organic
matter including bedding and manure. -- E. coli will infect mammary glands through environmental
contact. -- When E. coli bacteria die, a toxin is released; this toxin is the primary cause of the clinical
signs observed in a local mastitis infection. Antibiotics act to kill bacteria and in the case of these
infections, would then result in the toxin release. Therefore, intramammary antibiotic treatment is not a
generally recommended practice for local infections.”
In the 2011 bulletin, “Control of E. coli mastitis starts with vaccination,” Pfizer Animal Health, said,
“Research shows 60 percent to 70 percent of coliform mastitis infections become clinical.1 Coliform
mastitis, when it occurs, can become severe and cause these negative impacts on your cows:
Abnormal milk
Excessive udder edema
Dramatic drop in milk production

E. coli in Plants

In a 2002 study, “”Transmission of Escherichia coli O157:H7 from Contaminated Manure and
Irrigation Water to Lettuce Plant Tissue and Its Subsequent Internalization
, Ethan B. Solomon, et al.,
Rutgers University at New Brunswick, reported, “The transmission of Escherichia coli O157:H7 from
manure-contaminated soil and irrigation water to lettuce plants was demonstrated using laser scanning
confocal microscopy, epifluorescence microscopy, and recovery of viable cells from the inner tissues of
plants. E. coli O157:H7 migrated to internal locations in plant tissue and was thus protected from the
action of sanitizing agents by virtue of its inaccessibility. Experiments demonstrate that E. coli
O157:H7 can enter the lettuce plant through the root system and migrate throughout the edible portion
of the plant.”

In the 2011 study, “
Identification of the Cellular Location of Internalized Escherichia coli O157:H7 in
Mung Bean, Vigna radiata, by Immunocytochemical Techniques
,” Amanda J Deering, et al., Purdue
University, said, “Escherichia coli O157:H7 has been associated with numerous outbreaks involving
fresh produce. Previous studies have shown that bacteria can be internalized within plant tissue and that
this can be a source of protection from antimicrobial chemicals and environmental conditions.
However, the types of tissue and cellular locations the bacteria occupy in the plant following
internalization have not been addressed. In this study, immunocytochemical techniques were used to
localize internalized E. coli O157:H7 expressing green fluorescent protein in germinated mung bean
(Vigna radiata) hypocotyl tissue following contamination of intact seeds. An average of 13 bacteria per
mm(3) were localized within the sampled tissue. The bacteria were found to be associated with every
major tissue and corresponding cell type (cortex, phloem, xylem, epidermis, and pith). The cortical
cells located on the outside of the vascular bundles contained the majority of the internalized bacteria
(61%). In addition, the bacteria were localized primarily to the spaces between the cells (apoplast) and
not within the cells. Growth experiments were also performed and demonstrated that mung bean plants
could support the replication of bacteria to high levels (10(7) CFU per plant) following seed
contamination and that these levels could be sustained over a 12-day period. Therefore, E. coli
O157:H7 can be internalized in many different plant tissue types after a brief seed contamination event,
and the bacteria are able to grow and persist within the plant.”

In a
Droffner and Brinton study (1995), "It was observed that Salmonella and E. coli survived for 59 days at about 60
degrees C in an industrial compost." However, they reported, "The bacteria became undetectable after the
temperature decreased from 62 degrees C to about 40 degrees C in the compost curing."

Modern Surgery, General and Operative: General and Operative - Google Books Result
by John Chalmers Da Costa - 1919 - 1515 pages
Bacillus coli communis. pneumonia. The Bacillus coli communis, called also the Bacterium coli commune, the <olon
bacillus, or the bacillus of Escherich (Fig ...

Modern Surgery By John Chalmers Da Costa 1919

Other Surgical Microbes p. 61

The Bacillus coli communis, called also Bacterium coli commune, the colon bacillus, or the bacillus of Escherich was
discovered in feces by Emmerich in 1885. Under ordinary conditions this is a putrefactive bacillus inhabiting the
intestinal canal and feces invariable contains it. It is found in the mouth, nose, and vagina, on the skin, and under the
nails. The bacillus is normally found in water, even in water regarded by users as pure. It has already been stated that
this ordinarily harmless micro-organism may, under certain conditions, acquire pathogenic power and enter the
circulation. This bacterium grows best in air, but it can also grow when air is excluded.

This bacillus may be responsible for appendicitis, peritonitis, inflammation of the genito-urinary tract, pneumonia,
inflammation of the intestine, leptomeningitis, perineal abscess, cholangitis, cholecystitis, myelitis, puerperal fever,
wound infections and septicemia. It is the cause of many abscesses about the intestine and responsible for many
ischiorectal abscesses. From the pus of an appendicitis abscess we may perhaps obtain culture of Escherich's bacillus,
but usually find also streptococci or staphylococci, and sometimes pneumococcus.  Colon bacilli introduced into the
system by tainted food may be responsible for epidemic pneumonia . A few years ago there was such an epidemic in
Middlesbrough, England (Oliver, in "Brit. Med. Jour." April 30, 1910)

There is a misconception that  E. coli in the body is harmless. Before you believe that you need to read the story of
Lovella Thompson  who loss her feet and is missing part of all 10 fingers because of E. coli that never got out of her

Drug resistant genes are also inserted as markers in genetically engineered bacteria. Since there has been such a
dramatic increase in drug resistant bacteria in the last 25 to 30 years, there is a common (scientific and public) theory
that genetic engineers are responsible for a major portion of the increase. In fact, that theory may have some validity
since a patent was assigned to Stanford University in 1980 for a process to insert genes into non-disease causing E.
coli so as to create a bacteria never before seen in nature. Since that time E. coli has been the workhorse of genetic
engineering." "It is an accepted "fact" that the use of antibiotics in humans and cattle create drug resistant bacteria.
However, there is a caveat,  a USDA investigation in 1982 did not find 0157:H7 in any cattle in the United States."
"Scientists as well as EPA have known since the 50s that bacteria exchange DNA and genes in the treatment plant and
spit out drug resistant bacteria in the sewage effluent water and are concentrated in the sewage biological solids in

It would apear that, "
Sometimes prior to 1975, E. coli picked up a Shigella toxin gene unique to an epidemic in Central
America. Only the toxins produced by tetanus and botulism are more dangerous. California researchers identified 20
cases of this unique strain of Shigella during 1969/70 in a retrospect study in 1972.  The first E. coli 0157:H7 case (a
Naval Officer) documented with samples at CDC was in Oakland, California in 1975.  The Shigella like toxin  (a known
neurotoxin that produces delayed limb paralysis and death) was sequenced in 1986.  It was noted that Escherichia coli
of various serotypes, Salmonella typhimurium, and Vibrio choterae also produce the toxin. Researchers at Walter Reed
Hospital had cloned the toxin producing gene by 1987."

E. coli articles
Hydrogen Sulfide-Producing Variants of Escherichia coli
Myron D. Maker and John A. Washington II
Section of Clinical Microbiology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901


Seventeen strains of H2S-producing variants of Escherichia coli were isolated from specimens submitted for
microbiological study (ten from stool, five from urine, and two from postmortem material). Production of H2S was
unstable in several strains; however, other than their production of H2S, all strains closely resembled typical E. coli in
their biochemical reactions. In vitro susceptibilities of the H2S-producing variants to antimicrobics closely resembled
those of typical E. coli in this laboratory.

The biochemical and serological characteristics of more than
200 H2S-positive variants of E. coli were recently
reported by Darland and Davis (1).

It is conceivable, therefore, that a plasmid that mediates drug resistance or enterotoxin production can become linked
with H2S production. Enterotoxigenicity by strains of' E. coli (2) and other
Enterobacteriaceae (7) is now well known,
as is the high rate of transfer (6).
Appl Environ Microbiol. 1974 August; 28(2): 303-305

An H2S-producing variant of Escherichia coli (strain 142) isolated from a urinary tract infection was found to be
resistant to high levels of tetracycline, ampicillin, streptomycin, and sulfonamide. The H2S trait segregated
spontaneously at a frequency of 2.5 x 10-3. No segregation was observed for the drug resistance determinants. Neither
ethidium bromide nor acridine orange affected the rate of segregation of the drug resistance determinants or the trait
for H2S production. Antibiotic resistance and hydrogen sulfide production were conjugally transferred to E. coli K-12
recipients at a frequency of approximately 1i-5 per donor cell. Antibiotic resistance and hydrogen sulfide production
were also transduced as a single unit with phage P1L4. Genetic data, based on the segregation of resistance
determinants and the H2S trait among transconjugant and transductant classes, suggested the presence of two R
plasmids. Plasmid DNA was isolated by cesium chloride-ethidium bromide centrifugation. Two plasmid species were
detected by agarose gel electrophoresis of purified plasmid DNA, a large molecule of about 80 x 106 daltons
(designated pSR12) and a small molecular species of approximately 5.5 x 106 daltons (designated pSR13).
Transformation studies using purified plasmid DNA showed that the large pSR12 plasmid confers resistance to
ampicillin, tetracycline, and streptomycin and also carries the gene(s) for H2S production. The small pSR13 plasmid
confers resistance to streptomycin and sulfonamide.
Infections caused by ESBL-producing E. coli are a growing worldwide phenomenon and are not unique to the UK .
The figure being quoted in the media of 30,000 cases of infection due to ESBL-producing E. coli each year in the
UK is an estimate. The Health Protection Agency is one of the leading institutions worldwide in terms of research into this
area and has been providing advice about these infections for many years and, in particular, produced a report on the
increasing frequency of these infections in 2005.

The kinds of infections that ESBL-producing E. coli can cause range from urinary tract infections, to - at the more
serious end of the spectrum - cases where they enter the bloodstream and cause blood poisoning. Infections with
ESBL-producing E. coli are most common amongst the elderly, or those who have recently been in hospital or
received antibiotic treatment. ESBL-producing E. coli are extremely rare in simple cystitis.


Escherichia coli: (Coliform -- fecal coliform)  E. coli is unique in that the most deadly bacteria  0157:H7
only ferments lactose at 25°C (77°F) , while the coliform test is for bacteria that ferment
lactose at 35°C (95°F ), and the fecal coliform test is for a
thermotolerant E. coli bacteria
that ferments lactose at 44.5°C. (112.1°F)

E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7
serotype is negative for invasiveness (sereny test), elaborates no colonization factors (CFA/I or CFA/II),
Doesn't produce heat stable or heat labile toxins and is non-hemolytic. In addition, E. coli O157:H7 is usually
sorbitol negative whereas 93% of all E. coli ferment sorbitol.[6] E. coli O157:H7 also lacks the ability to
hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG)[7] and does not grow at 45 °C in the presence of
0.15% bile salts. Because of the latter characteristic this serotype cannot be isolated by using standard
fecal coliform methods that include incubation at 45 °C.[7][8]"

The International Escherichia and Klebsiella Centre (WHO) has a very large strain collection of
approximately 60,000 E. coli strains, most of which are clinical isolates. This collection includes test and
reference strains for O, K, H and F antigens, various toxins and other E. coli virulence factors. The
collection contains strains representing almost any possible sero- and virulence type.

The current  public relation ploy is that because E. coli is a part of the normal gut flora it is
not harmful to humans. However, once E. coli leaves the gut it can be very deadly as in urinary
tract infection or cause sepsis and meningitis in newborns.

As a group E. causes inflammatory diarrhea
, destruction of red blood cells and kidney
failure (hemolytic-uremic syndrome), urinary tract infections, bacteremia, meningitis,
severe, lung infection , pneumonia, abscesses  in the lining of the lungs (empyema),
necrotizing "flesh eating"  infections in the urinary tract and the abdominal cavity.

0157:H7 can not be treated with drugs, antibiotic-resistant.
Sequelae of ETEC, EPEC, and EIEC infection are not well described. Enteroaggregative E.
coli may cause chronic diarrhea.  There is no formal surveillance system for diarrheogenic
E. coli and most laboratories are unable to identify them.
Causes clinical mastitis in cattle.
Genome Project Information for a few E. coli strains

Escherichia coli 042 Facultative, Motile, Pathogen, Rod-shaped, Nonsporulating
Escherichia coli 101-1 Enteroaggregative, Pathogen, Facultative, Motile, Rod-shaped, Nonsporulating
Escherichia coli 536 Facultative, Motile, Pathogen, Rod-shaped, Nonsporulating
Escherichia coli 53638 Rod-shaped, Motile, pathogen, Nonsporulating, Facultative, Nonsporulating
Escherichia coli APEC O1 Pathogen, Rod-shaped, Motile, Facultative, Nonsporulating
Escherichia coli B Rod-shaped, Motile, Nonsporulating, Facultative, Non-Pathogen
Escherichia coli B171 Rod-shaped, pathogen, Facultative, Motile, Enteropathogenic, Nonsporulating
Escherichia coli B7A Rod-shaped, Facultative, Motile, pathogen, Enterotoxigenic, Nonsporulating
Escherichia coli CFT073 Facultative, Motile, Pathogen, Rod-shaped, Nonsporulating
Escherichia coli E110019 Rod-shaped, Motile, Facultative, pathogen,  Enteropathogenic, Nonsporulating
Escherichia coli E22 Rod-shaped, Motile, pathogen, Nonsporulating, Facultative, Enteropathogenic
Escherichia coli E24377A Pathogen, Enterotoxigenic, Rod-shaped, Motile, Facultative, Nonsporulating
Escherichia coli F11 Rod-shaped, Motile, pathogen,  Facultative, Enterotoxigenic, Nonsporulating
Escherichia coli HS Rod-shaped, Motile, Facultative, Pathogen, Nonsporulating
Escherichia coli K12 Facultative, Motile, Non-Pathogen, Rod-shaped, Nonsporulating
Escherichia coli O157:H7 EDL933 Pathogen, Facultative, Motile, Rod-shaped, Nonsporulating
Escherichia coli O157:H7 str. Sakai Pathogen, Facultative, Motile, Rod-shaped, Enterohemorrhagic, Nonsporulating
Escherichia coli SECEC SMS-3-5 Rod-shaped, Motile, pathogen, Nonsporulating, Facultative, Ciprofloxacin resistant, Moxifloxacin
Escherichia coli UTI89 Facultative, Motile, Pathogen, Rod-shaped, Nonsporulating

Journal of Food Protection
Article: pp. 1365–1370 | Abstract
Volume 67, Issue 7 (July 2004)

Persistence of Enterohemorrhagic Escherichia coli O157:H7 in Soil and on Leaf Lettuce and Parsley Grown in Fields
Treated with Contaminated Manure Composts or Irrigation Water

1. Center for Food Safety, University of Georgia, 1109 Experiment Street, Griffin, Georgia 30223-1797, 2. Department
of Horticulture, University of Georgia, Coastal Plain Experiment Station, Tifton, Georgia 31793, 3. Animal Waste
Pathogens Laboratory, U.S. Department of Agriculture, Agricultural Research Service, Beltsville Agricultural Research
Center, 10300 Baltimore Avenue, Building 001, Beltsville, Maryland 20705-2350, 4. Department of Food Science and
Human Nutrition, Clemson University, Clemson, South Carolina 29634, USA

Outbreaks of enterohemorrhagic Escherichia coli O157:H7 infections associated with lettuce and other leaf crops have
occurred with increasing frequency in recent years. Contaminated manure and polluted irrigation water are probable
vehicles for the pathogen in many outbreaks. In this study, the occurrence and persistence of E. coli O157:H7 in soil
fertilized with contaminated poultry or bovine manure composts or treated with contaminated irrigation water and on
lettuce and parsley grown on these soils under natural environmental conditions was determined. Twenty-five plots,
each 1.8 by 4.6 m, were used for each crop, with five treatments (one without compost, three with each of the three
composts, and one without compost but treated with contaminated water) and five replication plots for each treatment.
Three different types of compost, PM-5 (poultry manure compost), 338 (dairy manure compost), and NVIRO-4 (alkaline-
stabilized dairy manure compost), and irrigation water were inoculated with an avirulent strain of E. coli O157:H7.
Pathogen concentrations were 107 CFU/g of compost and 105 CFU/ml of water. Contaminated compost was applied to
soil in the field as a strip at 4.5 metric tons per hectare on the day before lettuce and parsley seedlings were
transplanted in late October 2002. Contaminated irrigation water was applied only once on the plants as a treatment in
five plots for each crop at the rate of 2 liters per plot 3 weeks after the seedlings were transplanted.
E. coli O157:H7
persisted for 154 to 217 days in soils amended with contaminated composts and was detected on lettuce
and parsley for up to 77 and 177 days, respectively, after seedlings were planted. Very little difference was
observed in E. coli O157:H7 persistence based on compost type alone. E. coli O157:H7 persisted longer (by
>60 days) in soil covered with parsley plants than in soil from lettuce plots, which were bare after lettuce
was harvested. In all cases, E. coli O157:H7 in soil, regardless of source or crop type, persisted for >5
months after application of contaminated compost or irrigation water.


EID Journal Home > Volume 13, Number 8–August 2007

Volume 13, Number 8–August 2007
PCR versus Hybridization for Detecting Virulence Genes of Enterohemorrhagic Escherichia coli

Robert S. Gerrish,* James E. Lee,* June Reed,* Joel Williams,* Larry D. Farrell,* Kathleen M. Spiegel,* Peter P. Sheridan,
* and Malcolm S. Shields*
*Idaho State University, Pocatello, Idaho, USA

Suggested citation for this article

We compared PCR amplification of 9 enterohemorrhagic Escherichia coli virulence factors among 40 isolates (21 O/H
antigenicity classes) with DNA hybridization. Both methods showed 100% of the chromosomal and phage genes: eae,
stx, and stx2. PCR did not detect 4%–20% of hybridizable plasmid genes: hlyA, katP, espP, toxB, open reading frame
(ORF) 1, and ORF2.

Enterohemorrhagic Escherichia coli (EHEC) pathogenicity is usually linked to a Shiga toxin (1,2) and virulence factors,
including adhesins, toxins, invasins, protein secretion systems, iron uptake systems, and several unidentified functions
(3,4), which are unrelated to strain phylogeny. In many laboratories, sorbitol-MacConkey medium is commonly used to
screen for the slow sorbitol fermentation phenotype of the most common Shiga toxin–containing strain: O157:H7 (5), but
this process does not address the pathogenic potential of the remaining sorbitol-positive E. coli. These organisms can
be detected by immunologic methods or PCR evaluation of virulence factors. PCR is the most useful method for
virulence factor detection, and others have made convincing arguments for its use in characterizing the virulence factor
patterns of potential pathogens (6,7).

Variation in virulence factor targets and use of different PCR primers contribute to variable results in detecting the most
common virulence factors: stx1, stx2, eae, and hlyA (or ehxA). Variation in amplification success is likely to increase
because more virulence factor variants are certain to emerge as more EHEC and Shiga toxin–producing E. coli (STEC)
strains are identified. This study addresses the potential for a broad and well-characterized set of control strains relative
to virulence factor amplification and confirmed by Southern hybridization.
It is
EPA's contention that E. coli only cause:

2.     Escherichia coli (pathogenic strains): ---------Gastroenteritis.

The Cytotoxic Necrotizing Factors (2007)  from Yersinia pseudotuberculosis and from Escherichia coli Bind to Different
Cellular Receptors but Take the Same Route to the Cytosol

The pathogenic groups includes enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E.
coli . ETEC may produce a heat-labile enterotoxin (LT) that is very similar in size (86 kDa), sequence, antigenicity, and
function to the cholera toxin (CT). EIEC closely resemble Shigella and causes an invasive, dysenteric form of diarrhea in
humans (6). Like Shigella, there are no known animal reservoirs; hence the primary source for EIEC appears to be
infected humans. Pathogenicity of EIEC is primarily due its ability to invade and destroy colonic tissue. EPEC causes a
profuse watery diarrheal disease and it is a leading cause of infantile diarrhea in developing countries. EHEC are
recognized as the primary cause of hemorrhagic colitis (HC) or bloody diarrhea, which can progress to the potentially
fatal hemolytic uremic syndrome (HUS). The infectious dose for O157:H7 is estimated to be 10 - 100 cells; but no
information is available for other EHEC serotypes.

One of the group of Enterobacteriaceae which includes: Enterobacter, Escherichia, Klebsiella, Morganella, Proteus,
Providencia, Salmonella, Serratia, Shigella, and Yersinia.

Bloody, watery, or inflammatory diarrhea (traveler's diarrhea). In children, diarrhea caused by certain strains of E. coli
may lead to destruction of red blood cells and kidney failure (hemolytic-uremic syndrome). E. coli can also cause urinary
tract infections (particularly in women) and bacteremia and meningitis in newborns (particularly premature newborns).
May cause severe, lung infection , pneumonia, may lead to the formation of abscesses (collections of pus) in the lung or
in the lining of the lungs (empyema).may cause deep infections, particularly in the urinary tract and the abdominal
cavity. (Merck)

Gonzalez E A, Blanco J. Serotypes and antibiotic resistance of verotoxigenic (VTEC) and
necrotizing (NTEC) Escherichia
coli strains isolated from calves with diarrhoea. FEMS Microbiol Lett. 1989;51:31–36. [PubMed]

Food Microbiology
Volume 16, Issue 1, February 1999, Pages 83-91  

Copyright © 1999 Academic Press. All rights reserved.

Regular Article
Differences in thermotolerance of various Escherichia coli O157:H7 strains in a salami matrix*1

G. Duffya, D. C. R. Riordana, 1, J. J. Sheridana, B. S. Eblenb, R. C. Whitingb, I. S. Blairc and D. A. McDowellc
a The National Food Centre, Teagasc, Castleknock, Dublin, 15, Ireland
b Eastern Regional Research Centre, Agricultural Research Service, 600 East Mermaid Lane, Wyndmoor,
Pennsylvania, 19038, USA
c University of Ulster, Newtownabbey, Anrim, BT37 0QB, Northern Ireland
Received 12 March 1998.  Available online 12 April 2002.

Three strains of Escherichia coliO157:H7 (ATCC 43895, Ent C9490 and 380–94) were inoculated into salami and
heated in water baths at 50, 55 or 60°C. At intervals between 1 and 360 min, salami samples were removed from the
water bath and examined for the presence of survivingE. coliO157:H7. Samples were directly plated onto sorbitol
MacConkey (SMAC) agar, and onto tryptone soya agar (TSA) with SMAC overlay. The number of sub-lethally damaged
cells in each sample was estimated from the differences between the resultant direct (uninjured cells only) and overlay
(total recovery) counts. In samples heated at 50°C, the percentage of cell injury ranged from 71·8–88% for all strains. In
samples heated at 55°C the percentage of sub-lethally damaged cells in strains ATCC 43895 and Ent C9490 was
significantly higher (P< 0·001) at 97% than that observed in strain 380–94 (64%). Cell injury was not measured at 60°C.
There were significant differences between the derived decimal reduction times (D-values) related to the different
strains ofE. coliO157:H7, the heat treatment applied and the recovery/enumeration agars used. Significant interstrain
differences (P< 0·05) in thermotolerance were noted. Strain Ent C9490 was significantly more heat resistant at 50°C
and 60°C (D-values of 116·9 and 2·2 min, respectively), while at 55°C strain 380–94 was more thermotolerant (D-value
of 21·9 min). The implications of these findings for the design of studies investigating the heat resistance ofE. coliO157:
H7 in fermented meat environments are discussed.

*1 Portions of this research were presented at the Annual Meeting of the International Association of Milk, Food, and
Environmental Sanitarians, 30 June to 3 July 1996 in Seattle, Washington, USA.

Mention of brand or firm names does not constitute an endorsement by the US Department of Agriculture over others of
a similar nature not mentioned.

1 Corresponding author.



Answered By: actualwolf-ga on 07 Sep 2002 18:38 PDT


Preventing the spread of all types of verocytotoxin-producing E.coli
(VTEC) meat depends not so much on the temperature at which you store
it, but rather the temperature at which you cook it.

According to the Mustafa Khammash at the University of California at
Santa Barbara the ideal temperature for the growth of E.coli is 37
Celsius.  You can check out a Power Point Presentation of his study of
the Feedback Regulation of Bacterial Stress Response at:
There's a chart on the fourth page down.

According to the Insitute of Food Science and Technology temperatures
below -5 degrees Celsius may retard the growth of E.Coli, but the
organism will survive.

"Refrigeration below 5 deg C is thought to prevent growth of VTEC and
is an important hygiene measure. However, any organisms present are
likely to survive at these temperatures perhaps for several weeks."

The key to killing E.coli in meat is to thoroughly cook it at a
temperature of 68.3 Celsius (approx. 160 F) or higher, for at least
two minutes.

hope this helps,


FEMS Microbiol Lett, 1992 Sep 15, 75(2-3), 155 - 9 Serogroups of Escherichia coli strains producing cytotoxic
necrotizing factors CNF1 and CNF2; Blanco J et al.; The serogroups of 396 necrotizing Escherichia coli of human and
bovine origin isolated in Spain between 1979 and 1991 have been determined .
The 270 cytotoxic necrotizing factor
strains belonged to 22 different O serogroups; however, 84% (226 of 270) were of one of seven serogroups (O2, O4,
O6, O14, O22, O75 and O83) . Although necrotizing E . coli producing cytotoxic necrotizing factor 2 belonged to 28
different serogroups, only six of them (O1, O3, O15, O55, O88 and O123) accounted for 60% (76 of 126) of cytotoxic
necrotizing factor 2 strains . Furthermore, only 3% (4 of 126) of cytotoxic necrotizing factor 2 strains belonged to
serogroups most common among strains producing cytotoxic necrotizing factor 1 . The majority of necrotizing E . coli
producing cytotoxic necrotizing factor 1 were obtained from human extraintestinal infections, whereas cytotoxic
necrotizing factor 2 strains were isolated from stools of healthy and diarrhoeic calves.

Colibacillosis occurs as an acute fatal septicemia or subacute pericarditis and airsacculitis. It is a common systemic
disease of economic importance in poultry and is seen worldwide.

Baby Calf Health: Common Diarrheal Diseases
Colibacillosis - E. coli - Colibacillosis usually occurs in calves 1-10 days old. Typically, calves out of first calf heifers are
more susceptible. Other associated factors include seasonal variation, overcrowding and poor sanitation which allow
build up of organisms in calving pens. Milk pails and feeding equipment can become contaminated. Signs include
frequent and effortless diarrhea, pasted rear quarters, fluid or semisolid malodorous feces with chunks of partially
digested milk, rapid dehydration and weight loss, depression, anorexia, weakness, and death. Body temperature is
normal at first but subnormal as the disease worsens. Death can occur in 3-5 days. Mixed infections can occur along
with rota/corona virus and/or cryptosporidiosis. Illness can occur in up to 75 percent of calves on a farm, while death
losses can range from 10 to 50 percent in unvaccinated herds.

Disease prevention is primarily achieved by early, rapid ingestion of colostral antibodies. Hours matter. A recent study
showed that if colostrum was given 3 hours after infection with E. coli, the calves were protected against disease. If
colostrum consumption was delayed until 4 hours after infection up to 40 percent of the calves died. All calves became ill
if colostrum was given 5 hours after infection. E. coli bacterins used to prevent calf diarrhea are different from E. coli
mastitis bacterins. Monoclonal antibodies work if given early (immediately after birth). Antibodies against E. coli antigens
have little effect once the diarrhea has commenced, they are principally prophylactic.