Jim Bynum, VP, and Gail Bynum, Ph.D
Help for Sewage Victims

In reviewing the large body of literature, it is virtually impossible for anyone to believe regulators and
scientists involved in the water and wastewater industry could not be aware coliform bacteria are
disease causing organisms with the potential to kill humans as well as animals. On the other hand,
some experts give out the impression that coliform is just the name of an EPA approved test. Coliform
were originally known as Bacillus coli or Colibacillus and finally Escherichia coli. E. coli and similar coli-
like-forms of colon bacteria became the family Enterobacteriaceae. These were the first recognized
bacteria. They were also the first known cause of disease.  E. coli is the primary coliform disease
causing organism with several strains becoming antibiotic resistant superbugs. E. coli 0157:H7 is not
only antibiotic resistant, drugs given for treatment will actually cause it to be more devastating. While
there is a debate about how many individual bacteria are needed to cause disease, the reality is that
only one is needed that multiplies every 20 minutes.  In the three to 7 day incubation period of a
disease, one bacteria becomes billions. The
Statens Serum Institut of Denmark has a strain bank
containing over 60,000 clinical E. coli strains that can multiply every 20 minutes under the appropriate
conditions.  The Material Safety Data Sheet (MSDS) furnished to researcher states, "All E. coli are
Hazard Group 2 bacteriological agents except E. coli O157:H7 [which is] (Group 3)". The Biosafety
level groups are for laboratory reference only, because biological agents were never expected to be
deliberately spread in communities under the guidance of federal agencies.

The most notorious coliform requiring Biosafety level group 3 laboratory practices is
Yersinia pestis
which causes the bubonic, pneumonic, and septicemic plagues. It is better known as the Justinian's
Plague of the 6th century. It was known as the Black Plague of the middle ages which is estimated to
have killed about 100 million people and the China plague of the late 19th and early 20th century
which spread around the world killing upward of 12 million people. In the last few years drug resistant
strains have surfaced. In 2005 there was an average of 13 plague cases annually in the Western

Yet, the Environmental Protection Agency
(EPA) in referring to the aftermath of Katrina flooding in
New Orleans states "coliforms generally do not pose a danger to people or animals, but they indicate
the presence of other disease-causing bacteria, such as those that cause typhoid, dysentery,
hepatitis A, and cholera." As EPA defines them, "Coliforms are bacteria that live in the intestines of
warm-blooded animals (humans, pets, farm animals, and wildlife). Fecal coliform bacteria are a kind of
coliform associated with human or animal wastes. Escherichia coli (E. coli) is part of the group of fecal
coliforms." Furthermore, in the basic information for the
Total Coliform Rule EPA states,  "When the
news media announce a "boil water emergency," reporters often speak of a "total coliform violation."
Coliforms are a group of bacteria, most of which are harmless. At first glance, it might seem strange
that a harmless group of bacteria such as coliforms could cause such commotion. But like police tape
and chalk outlines, coliform bacteria are often found at the scene of a crime even though they are not
themselves criminals."

EPA claims, "Protecting human health is an integral part of EPA's mission",  we can understand
why EPA does not want to cause a national panic while it is promoting the spreading of these disease
causing organisms on our food crops in sludge/biosolids, in our water as coliform and on our parks,
school grounds and lawns in reclaimed waster and compost. Typhoid (now known as enteric fever) is
actually caused by the coliform Salmonella typhimurium. The case of Typhoid Mary (Mary Mallon) in
1906 was the first indication healthy humans could be carriers of disease causing organisms without
any symptoms or illness. Now we know that many of us can carry chronic infections with little outward
harm. As noted with the Black Plague, many can walk through the middle of a pandemic with total

Dysentery is caused by the coliforms Salmonella and E. coli as well as other bacteria such as Vibiro
Cholera that don't show up in the coliform test. There are at least 30 clinical important coliform
members of the
Enterobacteriaceae family. They all release endotoxins, enterotoxins, and exotoxins
which can cause breaches in the stomach lining, destroy stomach cells and cause a cascade of organ

Despite spreading these known disease organisms around the environment, in our water and on our
food, the EPA Office of Inspector General stated in a 2002
"Status Report on Land Application of
Biosolids" that "EPA officials said investigating health impacts from biosolids is not an EPA
responsibility; rather, they believe it is the responsibility of the National Institute of Occupational
Safety and Health, the Centers for Disease Control, and local health departments." Not only that but,
EPA's "Compliance and Enforce has disinvested from the program." In effect, EPA has refused, and
still refuses, to investigate any human health effects caused by these disease organisms.

Yet, EPA allows drinking water treatment plants to fail 5% of the required monthly coliform tests.
Moreover, EPA claims sludge/biosolids is safe on agricultural and grazing land if there are less than 2
million E. coli colonies at the end of the fecal coliform test. As we documented in the
previous chapter,
the fecal coliform test has nothing to do with fecal contamination. The fecal coliform test only
enumerates a few thermotolerant strains of E. coli and Klebsiella that show some activity at 112.1°F.
Not only that but the coliform and fecal coliform tests suppress the growth of gram negative disease
causing bacteria EPA does not want to find.

According to modern textbooks there are only three pathogenic types of E. coli. The three pathogen
types cause, urinary tract infections (UTI), neonatal meningitis, and intestinal diseases
(gastroenteritis).  The first two types are caused by the common enteric E. coli that finds a way out of
the lower intestine and colon where they can also damage other organs. There are five
acknowledged types that may be involved in gastroenteritis, enterotoxigenic E. coli (ETEC),
enteroinvasive E. coli (EIEC), enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC),
and enteroaggregative E. coli (EAEC).

The Food and Drug Administration
(FDA), states, "the term "coliform" was coined to describe this
group of enteric bacteria", such as  
E. coli, Citrobacter, Klebsiella and Enterobacter. Moreover, they
are members of the "family Enterobacteriaceae, which includes many genera, including known
pathogens such as
Salmonella, Shigella, and Yersinia."  Furthermore, FDA states in Chapter 4 of the
Bacteriological Analytical Manual, "Although most strains of
E. coli are not regarded as pathogens,
they can be opportunistic pathogens that cause infections in immunocompromised hosts. There are
also pathogenic strains of E. coli that when ingested, causes gastrointestinal illness in healthy
humans. --- Coliform is not a taxonomic classification but rather a working definition used to describe
a group of Gram-negative, facultative anaerobic rod-shaped bacteria that ferments lactose to
produce acid and gas within 48 hours at 35°C. In 1914, the U.S. Public Health Service adopted the
enumeration of coliforms as a more convenient standard of sanitary significance."

Medical experts and microbiologist know coliform members of the Enterobacteriaceae family are
disease causing organisms. McGraw-Hill's 2002 Concise Dictionary of Modern Medicine states
Enterobacteriaceae are "distributed in nature in plants and animals, and are important pathogens," -
"they cause ±1⁄2 of all nosocomial infections in the US, most commonly by
Escherichia, Enterobacter,
Klebsiella, Proteus, Providentia, and Salmonella spp; less pathogenic Enterobacteriaceae include
Citrobacter, Edwardsiella, Erwinia, Hafnia, Serratia, Shigella, Yersinia spp." According to Western
Kentucky University's
genera belonging to the Enterobacteriaceae family have earned a reputation placing them among the
most pathogenic and most often encountered organisms in clinical microbiology. These Gram-
negative rods are usually associated with intestinal infections, but can be found in almost all natural

However, these are not the only coliform disease causing organisms. Medical studies find the disease
causing coliform bacteria:
Averyella, Budvicia aquatica, Buttiauxella noackiae, Calymmatobacterium,
Cedecea, Kluyvera, Koserella, Leclercia adecarboxylata, Leminorella, Moellerella wisconsensis,
Morganella, Pantoea, Photorhabdus, Rahnella aquatilis, Tatumella, Xenorhabdus and Yokenella

Historical Studies Showing Coliform Are Disease Causing Organisms

In 1884, Dr. Eugene A. Darling, Harvard Medical School, reported on Escherich's experiment which
found that B. coli from normal feces was fatal to rabbits and guinea pigs. Large amounts cause the
animal to become drowsy, stupid and exhibit diarrhea symptoms. Twenty-four to 48 hours later they
became paralyzed, comatose resulting in death. A quick death was generally from a bloodborne
infection while some infections resulted in slow paralysis with death in 12 to 49 days.
B. coli isolated from gastroenteritis was generally more virulent than from feces. It was thought that B.
coli in low doses were rarely fatal to animals and should not be considered virulent under normal

It has taken over 100 years to verify some of the medical observation made in 1899 by Albert G.
Nicholls, M.D., Demonstrator of Pathology, McGill University who reviewed the studies on kidney
infection. He wrote, "Acute inflammation of the kidneys is now said to be the result of
the following conditions":

    Further, all grades of severity exist, from a mild inflammation up to
    a true local suppurative [formation or discharge of pus] condition.
    The infection may be in some cases an ' ascending' one from the bladder,
    but more commonly a 'descending' one from the blood-stream.

    It is usual to teach that the acute cases may become chronic, and that the cirrhotic
    kidney is an end-stage of the chronic parenchymatous nephritis, or is due to arterial
    disease, or again, to certain poison, as alcohol, gout, and lead. (The "primare
    Schrumpfniere"' of the Vienna School. )

    And again, cirrhotic [degeneration of] kidneys may occur in children, where there could
    be no question of arterio-selerosis or chronic intoxications from mineral substances.

    Of the 32 acute forms of various kinds, bacteria, generally the specific
    germs of the disease, were found in 28. The overwhelming proportion
    of positive results leads me strongly to the conclusion that in the vast
    majority of cases, if not in all, acute nephritis is due to the presence of
    specific microbes.

    Of these one case, which was associated with Atrophic Cirrhosis of the liver, showed a
    few well marked minute diplococci with a halo. In two, one an alcoholic kidney, bacilli of
    doubtful nature were seen.
    As to the nature of these diplococcus forms, it may be said that they
    are identical in appearance and size with the diplococci which Adami has
    found recently in the liver, associated with progressive portal cirrhosis,
    and which he has proved to be a variant of the colon bacillus.

    He found diplococcus forms in all livers which stained a brownish hue and were probably
    dead forms, while in atrophic cirrhosis of the liver they were increased in number and
    stained well.

    That the process in chronic nephritis with productive inflammation
    is due to an embolic [blood] infection, is strongly supported by the histological
    features in the sections I have studied.

    In the great majority of the acute interstitial and acute mixed
    varieties, the areas of round-celled infiltration are to be found around the
    glomeruli or around the afferent vessels, and interlobular arterioles exactly
    as would be expected in an embolic infection. The same holds
    good for the chronic cases. In the arterio-sclerotic type, that the
    infiltration and proliferation is mostly confined to vascular districts needs
    only to he mentioned. In the early stages of the chronic diffuse nephritis
    one sees the inflammatory exudation in the same way about the
    afferent blood vessels, associated with connective tissue hyperplasia.

    Clinical evidence then strongly supports the view that Chronic
    Bright's Disease, and indeed Acute, may be a result of some long-standing
    gastro-intestinal disorder, 50 per cent, of cases giving this history,
    thirty per cent, of cases are insidious in onset, all the usual causes being
    absent: such might be called " Cryptogenetic forms." Can these be due
    to an infection from the intestine ?

    Macaigne, ( Me"d., Dec, 1896,) has published some important
    experimental observations. He has found that B. Coli derived
    from the healthy intestine is harmless in the abdominal cavity, but it
    becomes virulent if there is some disorder of the intestinal tract as diarrhea,
    constipation, strangulation, etc. He could produce nephritis in
    animals by intravenous innoculation with B. Coli but usually obtained a
    suppurative form.

    Anything then which causes a loss of the lining epithelium of the intestine
    with increased virulence of the germ, provides the starting point
    for a systemic infection. That this often happens is beyond doubt.
    The occurrence of pneumonia due to colon infection is well recognized
    in strangulated hernia, and in septic peritonitis due to the same germ,
    the bacillus coli has been found in all the organs of the body including
    the kidneys.

    In the light of the present study we get an entirely new conception of
    the process at work in the case of Bright's Disease. All cases, acute and
    chronic, are brought into the category of 'infections.' The nature of
    the infecting germ varies; in the acute forms it is usually the specific
    germ causing the primary disease although in some cases it is the colon
    bacillus. In the chronic cases, in the great majority, it is the colon
    which is the infective agent, but there is some evidence to favor the
    view that a few germs like the bacillus Pfeifferi and the diplococcus
    lanceolatus are capable of producing fibrosis. Two processes are at
    work, parenchymatous degeneration and productive inflammation.
    Parenchymatous degeneration alone is not to be regarded as a true
    nephritis, but is the result of chemical and bacterial toxins, bringing
    about injury to the secreting epithelium. Whether inflammatory infiltration
    occurs in addition or not depends on several factors.
    1st, the number and size of the infecting germs.
    2nd, the degree of virulence.
    3rd, their specific qualities.
    If the germs are few in number and of small size, they may pass
    through the glomerular capillaries, and merely produce degeneration and
    necrosis without further change. If they be sufficiently numerous to
    block the vessels or get into the capillary endothelium, then we get
    local inflammatory reaction with acute leucocytic infiltration.

Veranus A. Moore, State Veterinary College, Ithaca, New York, stated in a 1902 Committee report that:
    "(1) Many cultures of B. coli communis are fatal to guinea-pigs of 900 grammes weight
    when inoculated subcutaneously in doses of 1/4 to 1/2 Cc. of a fresh (24-hour) bouillon
    culture. Other cultures require the peritoneal injection of a like quantity of the virus for
    fatal results. (2) Some cultures do not produce morbid changes when injected in doses
    of 1 Cc. of the culture into the peritoneal cavity. (3) Cultures that have been isolated
    from the intestines of dogs have, in the writer's experience, been more virulent than
    those obtained from the normal viscera of other animals. (4) Although the colon bacillus
    appears to have become localized in the digestive tract of living animals, (including man)
    and to that extent become parasitic, it is not necessarily virulent as determined by animal
The report include tables for the reaction of B. coli from different animals their and their fermentation
of sugars and milk.

Joseph Coats, Professor Of Pathology In The University Of Glasgow reported in 1900 that while
B.coli was nonpathogenic in the colon, when the intestinal wall was penetrated B. coli caused an
infection in the thin membrane (peritonitis) that lines the abdominal wall that covers the internal
organs. It was also thought the peritonitis might be a result of an infection moving from the vagina and
uterus  Coats noted B. coli was often found in the liver and suggested it was one of the causes of

Edgar Macharg, Late Senior Assistant Physician, Belvidere Fever Hospital, Glasgow, relates his
findings in 57 cases of childbed fever that lasted over 24 hours. He noted that 31 patients died, while
only 26 recovered.  Many infections were due to rupture and/or injury of tissues during childbirth.
Infections included: inner lining of the uterus; infections within blood vessels; Meningitis --inflammation
of the membranes covering the brain and spinal cord;  the uterus lining, fallopian tubes, or ovaries;
inflammation of the small intestine; abscess; tissue that lines the wall of the abdomen and covers the
abdominal organs; and connective tissue adjacent to the uterus.
Bacillus coli, streptococcus
staphylocoocus pyogenes albus were the primary bacteria found.

T. Gillman Moorhead, Dublin Hospital, reviewed the history of B. coli group of colon bacteria in
1905. He noted that Escherich had described the bacteria in 1884 and shown that B. coli toxaemia
could be fatal to animals. However, Escherich thought it was harmless to man. Yet, by 1887, other
doctors had found that B. coli was pathogenic in wounds. Four years later colon bacteria had been a
proven cause of  (1) severe gastrointestinal disturbances , diarrhea, inflammation of the colon, and
other organ injuries; (2) inflammation of the stomach lining; (3) infected bile ducts; (4) urinary and
bladder infections; (5) lung diseases; (6) infection of heart and valves; (7) infections of the brain and
it's lining; (8) inflammation of bone joints . By 1905, the surgeons list had expanded with the addition
of (9) inflammation of the pancreas; (10) inflammation of the mammary gland (humans) or udder
(animals); (11) ear infections; (12) infections of the eyes; etc.

By 1906, Bacillus coli communis is acknowledge by the
United States Supreme Court to be an index of
fecal contamination in MISSOURI V. ILLINOIS, 200 US 496. Missouri was attempting to stop Chicago
from dumping sewage in a water way leading to the Mississippi River. Judge Holmes opinion states
that since both Missouri and Illinois dump sewage into the Mississippi River, each is responsibility for
cleaning up their drinking water supply. Otherwise, states downriver from Missouri would have a suit
against Missouri as well. As we documented in the
previous chapter, the test for Bacillus coli
incubated the sample for 24 - 48 hours at the optimum growth temperature of 37°C (98.6°F).

At about the same time Christiaan Eijkman suggested in 1906 that the only B. coli in feces from warm
blooded animals of any sanitary significance would grow when incubated at 46°C (114.8°F).  
However, the test for the total B. coli and other coli-like-forms of bacteria incubated at 37°C
(112.1°F) was adopted by the Public Health Service in 1914 and became known as the coliform test.  
The high temperature Eijkman test was accepted by the Public Health Service in 1964 with the
stipulation the sample would be incubated at a temperature of 44.5°C (112.1°C) and it was renamed
the fecal coliform test. This was only to be used as a field confirmatory procedure as some fecal
bacteria would be missed (
Salmonella, Shigella, etc.) and some nonfecal bacteria (Klebsiella) would
be included. The Public Health Service warned that "it is necessary to consider all fecal coliform
organisms as indicative of dangerous contamination." The current confirmatory procedure is to verify
the presence of E. coli and disregard all other coli-like-forms as well as all other noncoliform
pathogenic bacteria. It would be another 15 years (1979) before scientists discovered that less than
5% of the E. coli would show minimum growth at the higher temperature.

In 1909, Dr.
L. Van Es, Agricultural College, ND, read a paper on Colibacillosis at a meeting of the
Minnesota Veterinary Medical Association. Colibacillosis was first describe in 1799. By 1892,
scientists were focusing in on the normal intestinal B. coli as the primary disease causing organism for
which a vaccine was created. However, it was also noted that a number of bacteria species could also
cause fatal cases of diarrhea in calves. It was understood that B. coli was generally harmless because
it could not pass through the normal mucosa membranes that line the stomach and intestine, also
called epithelial cells. If there is any damage to this lining, bacteria can pass through causing infection
in blood and other organs. Since the mucosa lining is not fully form in new born humans and animals
and there is little formation of gastric acid, bacteria can easily enter the blood, heart and spleen. It
was noted that a vaginal infection could be passed on to the calf as well as infection of the udders (e.
g. mastitis). It is also possible for the infection to pass through the stump of the umbilical cord. Even
boiled milk could effect the mucosa and cause a fatal infection. Once the infection enters the blood
the fatality rate is about 80%. Treatment does little good. Surviving calves may suffer a relapse and
fail to thrive normally .

Lawrence, Kansas Daily World for Oct. 7, 1910 reported a Typhoid outbreak that caused one
death and 10 people suspected of having Typhoid fever. The typhoid bacillus Eberth was found in the
filth (manure, open toilets, slaughter products, etc.) in the infected ravine. Thirty private drinking
water wells were closed as some were within five feet and many were within 10 feet of the ravine.  
Authorities initiated a cleanup and threatened to pour kerosene in the private wells to prevent their
use, after another 20 drinking wells were closed. Karl Joseph Eberth had described the Typhoid
bacteria in 1882. Very seldom is the term Typhoid used any more since the name of the bacteria was
changed from Eberth to Salmonella typhi.

C.E.H. Milner, 4th London General Hospital, reported on a meningitis patient wounded in France in
1915. Splinters from a high explosive shell fractured the soldiers skull. While the wound had mostly
healed by the time he was brought to England, the soldier developed a high fever and there was a
small amount of cerebrospinal fluid still draining out. Milner recovered pure colonies of B. coli from the
spinal fluid, which he used to create a vaccine. Three days later the soldier's temperature dropped
and he had a normal recovery.

Alexis Thomson and Alexander  Miles' 1921 Manual of Surgery states B. coli invades any organ or
tissue where vitality is lowered. It causes localized lesions, cystitis, peritonitis, peritoneal suppuration
(or the formation of pus), appendicitis, also abscesses (localized collection of pus) in kidney,
suppuration in bile duct and liver, wounds have a fecal smell from putrefaction. B. coli is one of less
recognized bacteria that forms pus.

W.A. Newman Dorland updated "The American Illustrated Medical Dictionary" in 1922 with the
following list of diseases for Escherich's bacillus - (Theordor Escherich, German physician, 1857-
1911). The Bacillus coli.  [E. coli]
colibacillary -- produced by Bacillus coli
colibacillosis -- infection with Bacillus coli
colibacilluria - presence of colon bacillus in urine
colibacterin -- vaccine made from killed Bacillus coli used in treating cysitis, catarrhal jaundice and
various local infections.
colicysitis - cystitis dependant on the presence of the colon bacillus. [inflammation of the bladder]
colicystopyelitis - inflammation of the bladder and Kidney due to colon bacillus
coliform -- 1. Cribiform, 2. Resembling the Bacillus coli.
coli-group -- A group of bacteria, including Bacillus coli, the paracolon bacillus, typhoid bacillus
[e.g. Salmonella typhi], paratyphoid bacillus and bacillus of psittacosis -- influenza of
parrots that infects humans caused by E.coli or streptococcus -- paratyphoid fever
-- a continued fever with symptoms identical with those of typhoid fever but with
the Widal reaction negative. It is caused by a bacillus intermediate in form  [e.g.,
Salmonella paratyphi] between the typhoid bacillus and the colon bacillus --
paracolon bacillus.
coliysin - A lysin formed by Bacillus coli. [toxin]
colipyelitis - Pyelitis due to Bacillus coli [Acute inflammation ascending from kidney]
colisepsis - [blood inflammation] infection with Bacillus coli
colitis - inflammation of the colon
amebic c.  - colitis due to ameba coli
mucous c. -- a disease of the mucous membrane of the colon, marked by colic, constipation,
or diarrhea and the passage  of mucous and membranous shreds.
colitoxemia - Toxemia due to infection of colon bacillus.
coliuria --  Presence of the Bacillus coli in the urine

gas or gaseous gangrene -- gangrene in which hydrogen sulphid or other gas is formed in
   subcutaneous tissue, due to the action of Bacillus aerogenes [
Klebsiella] or Bacillus perfringens [Clostridium perfringens].

In a 1930 paper, Dr.
K. Douglas Wilkinson, reported that Bacillus coli was a common etiological agent
of urinary tract infections. Moreover, the symptoms were misleading and difficult to diagnose. There
are three stages of infections, acute, subacute, or chronic inflammation. The acute stage may be
mistaken for meningitis or pneumonia. The infections are often mistaken for appendicitis or abdominal
tuberculosis. He noted the infections could appear in the first week of life with the most fatalities
occurring to children under 2 years old. The greatest number of infections in boys and girls was
between the ages of 2 and 12. Out of 117 childhood cases studied, 7 of the nine (7.7%) deaths were
girls under two years of age.  Wilkinson recognized the ascending nature of the bacterial infection into
the bladder. More importantly, he found that some cases did not respond to treatment which led to
kidney damage and cardio-vascular damage. It is surprising to find that B. coli will actually grow at a
pH of 9.0. Urinary tract infections are often associated with gastroenteritis and chronically inflamed
appendix. Wilkinson was adamant that urinary tract infections were not associated with bloodborne
infections which included meningitis, pneumonia,  empyema, otitis media, acute infective enteritis and
jaundice. In adult women a urinary tract infection is common during pregnancy and especially after
the birth of a child. It is also common during or after a honeymoon as well as retaining urine during a
long trip without going to the toilet. It was pointed out during the discussion section of the published
paper that while streptococcus and staphylococcus was a major cause of kidney disease, B. coli
rarely did. However, it was not rare for young calves to developed B. coli kidney infections.

In 1934 study,
Edith E. Nicholls reported on the nature of hemolytic and nonhemolytic Bacillus coli
found in healthy individuals.  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 Anna Dean
Dulaney and I. D. Michelson, Medical School, University of Tennessee,
Memphis, An outbreak of neonatal diarrhea occurred at the Memphis General Hospital during the
winter of 1933-34 killing 47% of the babies. Symptoms appeared 5 to 9 days after birth. The babies
did not respond to any medication available. The predominate organism found was E. coli along with
Staphylococcus albus, and pneumococci. Strange colored stools contained slow lactose fermenting
bacilli referred to as B. coli mutabile. Three type of colonies were cultured: B. coli colonies;
enterococci; and the typhoid-dysentery group. The final observation was that the deaths might be
caused by a bacteria yet to be recognized.

According to a 1940 study by Drs.
Byron D. Bowen, M.D., AND Ernest Witebsky, Medical Service of
the Buffalo General Hospital, they had been involved with four cases of fulminating
Bacillus coli
septicemia, (e.g. sudden onset of severe infection in the blood). Three cases involved E. coli infection
and death within 3 days of entering the hospital.  The fourth case involved a blood infection by
Bacillus Aerogenes Capsulatus (
Aerobacter aerogenes, e.g. Enterobacter aerogenes and later
Klebsiella aerogenes) and Enterococci. According to their study, Septicemia caused by B. coli had
only been reported 110 times in the last 50 years. The death rate was 30 to 40 per cent. They noted
that while the textbooks described a clinical picture of blood infection by other bacteria such as
delirium, stupor and finally coma., they did not describe the same features for E. coli. The theory was
that the weak immunity of diabetics allowed a sudden invasion of bacteria from a urinary tract
infection. In this study all were obese diabetic subjects.

P. N.
Coleman and S. Taylor investigated the bacteria associated with urinary tract infection in 1949.
They found Bacteria aerogenes was resistant to sulphanilamide and to penicillin. They found that six,
out of 18 Bacteria aerogenes strains incubated at 44°C did not produce produced gas at 24 hours,
but they did produce gas at 48 hours. They also found P. vulgaris,  P. morgani and three paracolon
anaerogenic strains. Where there was no damage to the urinary tract, E. coli was the predominate
organism though there were 12 other organisms involved. Where surgery or some medical condition
was involved, E. coli was uncommon and replaced by P. vulgaris, P. morgani, and Bact. aerogenes.
When looking at 200 clinical cultures in 1929 from all types of infections 100 involved E. coli, 79
B. aerogenes and some proteus group. It was opined that E. coli was the most successful
bacteria at invading tissue.

In 1954, Dr. R.
Meyer reported on an abscess (pus pocket) in the knee of an 18 year girl. There was
no history of the girl being infected by E. coli. Meyer found a pus sac in the knee joint. Pure E. coli
cultures were grown from the pus. The E. coli was resistant to streptomycin and pencillin. However, it
was sensitive to cholomycetin. He noted the literature suggested that while abscesses, conjunctivitis
and invasion of body tissues had been observed, they were unusual.

Donald G. McKay and associates at the Departments of Pathology, Obstetrics and Gynecology,
Harvard Medical School, Boston, and the Pathology Laboratory, Free Hospital for Women,
Brookline, Mass. did some of the first work to understand the potential for endotoxins to cause blood
clotting in 1958. According to the textbooks, Endotoxins are part of the outer wall of all gram negative
bacteria, including those that are not generally considered pathogens. As the bacteria grow, some of
the cell wall endotoxins are released into the body as antigens, which may cause inflammatory
responses. Endotoxins are less potent than exotoxins which are released by some bacteria when they
die, which could be lethal as they could damage the stomach lining, disrupt nerve and cell functions
or kill the cells. The symptoms include fever, inflammation, blood clotting, hemorrhaging and even
toxic shock. Since this information was not known in 1958, McKay's work focused on whether
endotoxins had a direct or indirect effect on causing blood clotting. He found that as little as 0.005
mg/ml of purified endotoxin shortened the clotting time by 20%. At 1.0 mg/ml the clotting time was cut
in half. An unusual aspect of the research was finding that endotoxins did not cause clotting in
hemophiliac blood (hereditary non-clotting defect) when the sample was contained in glass, but it did
when the sample was contained in a silicone container.

Gaines and Joseph G. Tulley, in 1961, investigated the role of the endotoxin called "O"
antigen might have on  the virulence of the typhoid causing bacteria, Salmonella. They noted the
virulence  of the "O", like the Vi antigen was well known at that time.  They also noted the smooth cell
type bacteria with "O" antigen was more virulent than the rough type cell with little or no "O" endotoxin
in the typhoid bacteria. This is one of the few studies that identifies antigens as endotoxins.

In 1963,   
Claude DE LA Vaissiere and Bernard Goiffon described a procedure to use a fluorescence
microscope to quickly diagnose toxic gastroenteritis due to pathogenic colibacillus in infants. They
noted that the test used for identifying Escherichia coli enteropathogens usually took 24-48 hours
and the diagnoses is not normally received for another 2 days. They did acknowledge some E. coli
did not show up in the test.

Clive C.
Gay, University Veterinary Hospital, University of Glasgow, discussed Escherichia coli and
Neonatal Disease of Calves in a 1965 study. We find that colibacillosis is the term used for "calf
scours" and an acute septicemias infection (invasion of the bloodstream) caused by the coliforms
Escherichia coli and Salmonella as well as by Diplococcus, Pasteurella, and Streptococcus. Gay said
by the time the calf is 24 hours old the gut "flora is comprised mainly of E. coli, Streptococcus spp.,
and Clostridium perfringens, with Lactobacillus and Bacteroides species" Gay showed that the gut
flora of calves failing to receive the globulin fraction of colostrum was over run by E. coli causing their
death. Any calves that survived failed to grow normally. However, he acknowledge little was known
about how E. coli produced three different types of disease syndromes in calves. One interesting
point made was that K anigens (endotoxins) are extremely heat stable. L-type and B-type K antigen
take 100°C heat for 1 hour to be destroyed, while A-type K antigens require a temperature of 121°C
for 2 1/2 hours. Some E. coli have more than 1 type of K antigen.

One dose of the antibiotic Bacitracin was shown to kill more than 80% of guinea pigs in a 1966 study
by W. Edmund
Farrar, Jr.  and associates at Walter Reed Army Institute of Research. Gram positive
bacteria dropped 2,000 fold in the first 12 hours. Gram negative coliform bacteria increased 10 million-
fold, from less than 100 per gram to over a billion per gram within 48 hours. Coliform bacteria in the
blood was evident in 40% of the animals killed between 72 and 96 hours. The coliforms found were:
E. coli, Klebsiella-Aerobacter, and paracolon organisms including
Proteus. An unusual finding was
that high doses of Bacitracin actually inhibited the growth of coliform for about 24 hours.

Howard University infectious disease experts,
Vinod R. Mody and associates, compared the changing
nature of bacterial hospital infections over a 10 year period at Freedmen's teaching hospital in 1968.  
The based period was for adult infections during November and December 1965 and January 1966
compared to the same period in 1955-56. Over all, there was little change in the total number of
infections. There was a 14% increase in gram negative coliform bacterial infections during the 10
period for a total of 56%. There  was also a 14% drop in gram positive infections.  The biggest drop
was in the gram positive
Staphylococci and Streptococci infections. The largest increase was gram
negative E. coli infections. They evaluated the gram negative bacterial infections in 320 patients with
the following results.

Modern Studies Confirming the Historical Studies -- After EPA Was Created

Gram negative coliform bacteria contain inflammatory causing antigens which cause the immune
system to produce antibodies in an attempt to clear the foreign substances (e.g.,  bacteria, fungi,
parasites, viruses, toxins and other chemicals).
James W. Smith and Bertil Kaijser published their
research on E. coli K and O antigens spread through the blood in 1976. They focused on infections
of the kidney and the ureters. They found both local and serum antibody response was much less to
K-antigens than it was for O-antigens. Furthermore, K-antigens produced local immune responses in
less than half the animals infected. It was noted that antibodies to O-antigens developed in ascending
kidney infection, but did not develop in bladder infections. Moreover, the antigens remained in the
kidney long after bacteria could no longer be cultured. However, they were not sure how this effected
kidney destruction. The unusual finding was that E. coli urinary tract infection contained more
K-antigens than stools, or bladder infections, from the same patients.

In 1976,
M.S. Schiffer and associates reported there are 3 types of antigens (O, H, K) produced by E.
coli. E. coli with the encapsulated (smooth) K-antigen causes 80% of neonatal meningitis cases and
40% of the bacterial blood infections. They noted that more K-antigen strains were found in kidney
tissue than other types. Research also showed that smooth type K-antigen strains more likely to
cause a fatal infection than an unencapsulated (rough type) strains that were recognized by the
immune system and cleared from the blood. It would take another 27 years before K.J. Kim and
associates discovered the smooth type K-antigen strain could be enclosed in a membrane bubble
and passed through the blood-brain barrier without being recognized by the immune systems.

Jane Pitt, Columbia University College of Physicians and Surgeons, reviewed 137 cases of adult
patients with E. coli in their blood in 1979. She found that the average age of those with the E. coli K1
antigen in their blood was 54, while the average age of those with other antigens in their blood was
61. While none of the people with the E. coli K1 antigen in their blood died, 33% of those with other E.
coli antigens in their blood did. Women where the largest majority in both groups.

Dr. Lee W. Riley and associates reported on the first documented outbreak of E. coli 0157:H7 in
1983. There was an unusual aspect to this E. coli strain, it was not invasive or toxigenic by standard
tests. They noted the first sporadic case of hemorrhagic colitis was from a 1975 case. While they
neglected to mention it, the 1975 case was a Naval Officer from Oakland, CA. Perhaps, it is only a
coincidence that the Naval Biosciences Laboratory at Oakland was involved in the controversy over
recombinant DNA used to create bacteria never before seen in nature, such as E. coli 0157:H7. This
is just one of the antibiotic resistant coliform that will cause Hemolytic uremic syndrome (HUS) and
acute kidney failure. It should be mentioned that antibiotic treatment may trigger a release of
exotoxins that could cause a cascade of damage to organs and death.

Australian Veterans’ Entitlements Act of 1986 recognized that antigens are "toxins [e.g.,
Endotoxins, enterotoxins and exotoxins - which includes neurotoxins and cell killing Cytotoxins] and
foreign proteins, or particulate such as bacteria and tissue cells" which causes extrinsic allergic
alveolitis (Hypersensitivity pneumonitis) Extrinsic allergic alveolitis is associated with a restrictive
pattern of respiratory function tests."  Antigens sources of interest here are:
    · Detergent powder
    · Sewage sludge contaminated with micro-organisms
    · Sauna water contaminated with micro-organisms
    · Fertilizer contaminated with micro-organisms
    · Compost dust contaminated with micro-organisms

The Canadian Centre for Occupational Health and Safety fact sheet on extrinsic allergic alveolitis
illustrates why it is difficult to prove harm from the disease causing organisms and their toxins in
reclaimed water, sludge/biosolids and sludge/biosolids compost. Examples of different names for
Extrinsic Allergic Alveolitis disease caused by antigen toxins: "Sewage sludge disease; Wheat weevil
lung; Farmers' lung; Animal handlers' lung; Cheese washers' lung; Bagassosis; Hot tub lung; Air
conditioner lung;  Bird fanciers' lung; Maltworkers' lung; Maple bark strippers' disease; Mushroom
workers' lung; Wood pulp workers' disease; Sequoiosis; and Sequoiosis."

Edwin A. Deitch Department of Surgery, Louisiana State University Medical Center, read the
"Endotoxin Promotes the Translocation of Bacteria From the Gut", before the 6TH ANNUAL
paper was published in the Archives of  Surgery in 1987. This was followed up in 1989 when
Edwin A. Deitch and associates, further documented that endotoxins in the gut allows bacteria to
translocate through the stomach wall into the mesenteric lymph nodes. While
E. coli is the primary
bacteria found to translocate through the stomach wall to the lymph nodes,
Proteus, Enterococcus,
Pseudomonas, and Staphylococcus have also done so. When the mucosal barrier of the stomach wall
is breached by bacteria they may enter the blood and travel to other organs leading to sepsis (i.e..,
acute inflammation reaction throughout the entire body which may cause a cascade of organ
failures.). Any amount of E. coli endotoxin above 0.25mg killed 100% of the mice in the tests. E. coli
endotoxin injections of 0.05 mg was not lethal, but it allowed the mucosal barrier to be breached by
bacteria in 50% of the mice. They documented that a non-lethal dose of E. coli endotoxin altered
the mucosal barrier leading to multi-organ failure. Deitch said, "Furthermore, the combination of a
nonlethal dose of endotoxin plus a protein-malnourished state or a nonlethal thermal injury results in
lethal sepsis -- Endotoxin has a wide range of biologic actions, including the ability to modulate the
immune system, increase vascular permeability, impair cellular metabolism and oxygen utilization,
initiate disseminated intravascular coagulation, and produce profound hemodynamic changes
resulting in hypotension and death."

In the 1989 proposed sludge regulation Part 257 et al. (503) EPA released a list of
25 primary
pathogens in sewage sludge. The list was removed four years later from the final regulation. The
1989 proposed sewage sludge regulation only mentioned five bacteria of which three (2-3-4) are
Campylobacter jejuni ---------------------------   Gastroenteritis.
Escherichia coli (pathogenic strains): ---------Gastroenteritis.
Salmonella sp ------------------------------------- Gastroenteritis and enteric fever [Typhoid]
Shigella sp ----------------------------------------  Gastroenteritis.
Vibrio Cholerae ------------------------------------Cholera

Under the Resource Conservation and Recovery Act (
RCRA) sludge/biosolids containing these
infectious bacteria are classified as a hazardous waste because they may "(A) cause, or significantly
contribute to an increase in mortality or an increase in serious irreversible, or incapacitating
reversible, illness; or (B) pose a substantial present or potential hazard to human health or the
environment when improperly treated, stored, transported, or disposed of, or otherwise managed."

The average person would accept EPA's implied implication that there is no serious health effects
associated with the three coliforms. The implication is that the worse that could happen is an upset
stomach or perhaps some diarrhea and associated fever. Research shows that enteric fever is really
the benign name for Typhoid fever. If the disease is not properly diagnosed, Typhoid fever will
progress to delirium, loss of mental capacity, intestinal hemorrhage, bowel perforation, and death.  
According to Dr. Arthur Diskin, Vice-President, Global Chief Medical Officer, Royal Caribbean Cruise
Lines, gastroenteritis results in an estimated 100 million cases of acute diarrhea in the United States.
Diskin states, "210,000 pediatric hospitalizations occur yearly, with as many as 10,000 deaths."
Except for some laboratory cultivated strains, all E, coli are potential pathogens if they enter the blood
system (blood poisoning -- spreading infections into other organs)  or enter the body through the
urinary system (UTI), mouth and nose (intestinal diseases -- gastroenteritis). More than 200,000
people die each year from gram negative and positive bacterial sepsis (septic shock) -- the body's
exaggerated immune response to infections and foreign chemicals. Other than Typhoid, Salmonella
causes many of the same diseases as E. coli. The same is true for Shigella. An unusual aspect of
Shigella infection is that it may cause part of the rectum to be pushed out of the body. Permanent loss
of bowel control may result.

Tessy A. Joseph and associates from Department of Pediatrics, Cook County Children's Hospital
reported on the changes in infections of neonates with early-onset E coli infection born between 1982
and 1993. Their 1998 study showed a shift from a slow onset of E. coli ampicillin-sensitive bacterial
strains infecting  blood (sepsis),   to ampicillin-resistant strains that developed quickly, was intense
and severe to the point death (septic shock) could follow in the first 24 hours. They opined that this
was a result of  giving the mother ampicillin for fever during birth to prevent neonatal group B
streptococcal disease.

P. Brouqui and D. Raoult reported in 2001 on "Endocarditis Due to Rare and Fastidious Bacteria."
The gram negative bacteria they found were, the HACEK group of bacteria
Haemophilus species
(Haemophilus parainfluenzae, Haemophilus aphrophilus, Haemophilus paraphrophilus),
Cardiobacterium hominis, Eikenella corrodens, and Kingella species,
Campylobacter fetus, Pasteurella spp.,  Brucella spp., Bordetella spp.,  Francisella tularensis,  
Aeromonas hydrophila,  Streptobacillus moniliformis and the coliforms,
Yersinia enterocolitica, Salmonella spp., and Klebsiella spp.  They said, fastidious bacteria include:
Abiotrophia, HACEK group bacteria, Clostridium, Brucella, Legionella, Mycobacterium, and Bartonella
spp.. Moreover, rare bacteria associated with heart disease are:
Lactobacillus spp., Klebsiella spp.,
Corynebacterium, Salmonella, Gemella, Campylobacter, Aeromonas, Yersinia, Nocardia, Pasteurella,
Listeria, or Erysipelothrix spp.. Furthermore, slow growing bacteria such as the HACEK group,
Abiotrophia spp., Brucella spp., Bartonella spp., Legionella spp., and Mycoplasma spp. may not show
up in standard blood testing. The symptoms may suggest congestive heart failure, stroke caused by
emboli clots and bronchopneumonia. Exposure may be oral (including dental), sexual, surgical,
animals, employment and pests.

Niehaus reported on a case of Parkinsonism caused by Lipopolysaccharides [endotoxins]
of Salmonella Minnesota at the at the XIV International Congress on Parkinson's Disease in 2001.
A 22 year old laboratory worker was exposed to the endotoxin through an open wound on the thumb.
This resulted in a sepsis-like inflammatory reaction with flu-like symptoms and vomiting. Over time it
progressed to chronic inflammation of the central nervous system such as slowed ability to start and
continue movements, and impaired ability to adjust the body's position, rigidity, tremor, stiffness.

Lei Wang and associates from the School of Molecular and Microbial Biosciences, The University of
Sydney, Australia sequenced all of the 53 forms of the E. coli H-antigens in 2002. They supposed the
43 forms contained the fliC gene from the common ancestor E.coli/Salmonella. It was opined that the
other 10 forms were due to lateral transfer mutations. They note the H and O antigens were the best
understood components of E. coli clones and had been used for blood serotyping since the 1930s.

In 2002, The European Council of Applied Sciences and Engineering, an independent non-profit
organisation of national academies of Engineering, Applied Sciences and Technology from 21
European countries published a study by Dr.
Wolfram Martens and Prof. Dr. Reinhard Böhm,
Universität Hohenheim, on the public health aspects of the pathogens found in sludge. The primary
pathogenic coliform were
Salmonella spp.; Shigella spp.; Escherichia coli; and Yersinia enterocolitica.
The secondary pathogenic coliform were
Escherichia coli; Klebsiella; Enterobacter; Serratia;
Citrobacter; Proteus; Providencia. Most of these are Multiresistant bacteria.

It wasn't until 2003 that
K.J. Kim and associates, Division of Pediatrics Infectious Diseases, The Johns
Hopkins University School of Medicine, first demonstrated how, and why, the E. coli bacteria could
cross the blood-brain barrier to cause meningitis. Basically, E. coli K antigens as well as Salmonella,
Mycobacterium and Legionella are known to survive and multiply within a cell membrane bubble and
are not recognized by the immune system. The E. coli K antigens are devastating  killers of infants,
both humans and animals, but can be cleared from the blood of adults with proper treatment.

Also, In 2003,
R. MICOL and associates reported on 5 cases of native (heart) valve endocarditis
(NVE) caused by E. coli. They found that older people could develop acute heart disease from a
urinary tract infection which resulted in a high death rate. The E. coli were not a virulent clone, but the
normal urosepsis E. coli (group B2, papG allele II, siderophores.

Michael D.
Wheeler reported in 2004 on the science of endotoxins and liver disease. Endotoxins are
the cell walls of gram negative coliform bacteria. Cirrhosis of the liver has long been blamed on
excessive alcoholic consumption, but Wheeler shows that when bacteria in the gut die, endotoxins are
released which penetrate the walls of the gut and enter the blood stream leading to endotoxemia (i.e.,
adult respiratory distress syndrome (ARDS), hemorrhages, necrosis of the kidneys, and shock). .
When the endotoxins enter the liver, Kupffer cells are activated. The Kupffer cells release chemicals
leading to tissue damage in the liver.

Lidwien A.M.
Smit and associates studied the effects of endotoxins on wastewater treatment plant
workers who were only exposed 8 hours a day in 2005. They found three types of symptoms: ‘‘lower
respiratory and skin symptoms’’; ‘‘flu-like and systemic symptoms’’; and ‘‘upper respiratory symptoms.’’

Yufeng Yao and associates, Division of Pediatric Infectious Diseases, Department of Pediatrics,
School of Medicine, Johns Hopkins University, compared the gene grouping of 11 E. coli K1 antigen
strains taken from the spinal fluid of neonatal meningitis patients in 2006. Yao said, "Escherichia coli
is a major cause of enteric/diarrheal diseases, urinary tract infections, and sepsis." Sepsis is a term
doctors don't use much anymore. It is bacterial blood infection that is generally referred to as a
"complication" of infections that may start in any part of the body. The blood pressure will drop
resulting in a toxic shock to the body interrupting the function of all major organisms and the central
nervous system. Yao found that there were two groups within the 11 E. coli K1 antigen strains they
investigated that caused meningitis (i.e., E. coli O1, O7, O12, O16, O18 and O45). Each group used
a different mechanism. An unusual finding was that while the cytotoxic necrotizing factor 1 (cell killing
protein toxin) was known to be involved in meningitis, only two K1 strains investigated included this
protein toxin. Yao confirmed that the outer cell membrane of the gram negative Enterobacteriaceae
(coliform) contained Lipoprotein. This cell protein causes an immune system proinflammatory cytokine
storm which may lead to lethal toxic shock. The study notes mobile genetic islands as well as
individual virulence factors can be translocated by lateral transfer to other bacteria.

Martin Baumgart and associates at Cornell University found in a 2007 study that only about 30% of
the human fecal flora organisms could be cultured in the laboratory. The focus of the study was
investigating the cause of chronic debilitating colon inflammation known as Crohn’s disease. It has
been accepted that the disease is restricted to genetically susceptible individuals. A number of
bacteria have been implicated in Crohns's disease, but never substantiated. Part of the problem
appears to be that different bacteria may inhibit the final section of the small intestine (ileum) and the
lower bowel section (colon). Baumgart found that "a novel group of E. coli  contains opportunistic
pathogens" that may be the cause of Crohn;s disease in the ileum. He said, the novel group is similar
to "uropathogenic and avian pathogenic E. coli, and pathogenic Enterobacteriaceae"  (e.g., coliform).
The finding was based on the high numbers of novel invasive pathogenic E. coli found in the inflamed
intestinal mucosa lining.

In 2008,
Jeffrey T. Borenstein, Director of the Biomedical Engineering Center at Draper Laboratory,
reported on new information that bacterial clusters can trigger coagulation in the blood system. He
noted that many bacterial infections from
Staphylococcus aureus to Escherichia coli are known to
produce blood clotting factors that can lead to sepsis, septic shock and organ failure. This is a special
problem for those with compromised immune systems. His unusual finding was that bacteria evenly
distributed in the blood system did not cause blood clotting. However, when the bacteria congregated
and acted together, clotting factors were released and blood clots developed. It is interesting to note
Borenstien did not review any endotoxin studies such as Dr. McKay's 1958 discussion on the potential
for bacterial endotoxins to cause blood clotting.

According to
Isaac P Humphrey and associates (2009), heart valve infections were the result of gram
positive bacteria and the more virulent gram negative slow growing bacteria: "
Haemophilus species
(Haemophilus parainfluenzae, Haemophilus aphrophilus, Haemophilus paraphrophilus),
actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species." Tthey
state this group was referred to by the first letter of each bacteria, HACEK. They also cause infections
of: the mouth and gums, bacterial blood poisoning,  lining of the stomach, middle ear, outermost layer
of the eye, inflammation of the lung, arthritis, bones, urinary tract, wounds and brain absesses.
Humphrey noted 60 percent of the cases were a result of dental infections and most were subacute.
However, the vegetation created by the bacteria may break loose causing blood vessel blockage
leading to stroke, heart attack, kidney problems, bowel malfunction and focal pneumonia.

Karen J. Vigil and associates at the Medical School and School of Public Health, The University of
Texas Health Center reported in 2010 that a new type of  pus producing E. coli infection of the
skeletal muscles was emerging as a serious problem worldwide. This is a fluoroquinolone‐resistant,
ESBL‐positive E. coli. The disease has usually been caused by gram‐positive bacteria such as
Staphylococcus aureus.

Tarun Madappa, Department of Pulmonary and Critical Care Medicine, Elkhart General Hospital, and
Chi Hiong U Go, Department of Internal Medicine, Texas Tech University Health Science Center at
Odessa,  outline some of the diseases caused by E. coli in a September 2010 study published
online.  Diseases include: enteric infections, Arrhythmias (Tachycardia), psoas abscess appendicitis,
infectious arthritis, abnormally fast breathing (Tachypnea), brain abscess, confusion, diarrhea,  viable
bacteria in the circulating blood, infection of the biliary tract, inflammatory process of the bone and its
structures, Central Nervous System manifestations, enterotoxin, endotoxin disseminated intravascular
coagulation, fever, gastroenteritis, congestive heart failure  infection of the endocardial surface of the
heart, hemorrhagic colitis, hemolytic-uremic syndrome - kidney failure, hypotension, Jaundice, intra-
abdominal infections,   inflammation of the gallbladder, inflammatory reaction of the intraocular (eye)
fluids or tissues, liver abscess, meningitis, maternal peripartum (vaginal) infection, neonatal tetanus,
pneumonia, pulmonary embolism, prostatitis, respiratory tract infections, ruptured aneurysm, seizures,
shaking chills,  toxic shock symptomatic cystitis, inflammation of the sinuses, skin and soft-tissue
(necrotizing)  infections that kill tissue - interfere with blood flow - break down materials in tissue,  
inflammatory diseases of the thyroid gland, urinary tract infection, infection-induced inflammation of
the urethra, infection of the umbilical stump, death.

In July 2010, Dr. Jae Myung
Park, reported on the follow up studies on the Long-term Prognosis of
Postinfectious Irritable Bowel Syndrome from the massive 2000 acute gastroenteritis outbreak in
Walkerton, Canada. The town's water well was contaminated with Escherichia coli 0157:H7,
Campylobacter jejuni, and other pathogens. Over 2300 out of 4315 residents were infected. This
resulted in 27 cases of kidney failure and 7 deaths. The authors concluded that acute gastroenteritis
could trigger Irritable Bowel Syndrome symptoms which lasted over 8 years for 15.4% of those
infected. However, that number may be low because only 53.5% participants returned for the last
follow up of the study.

Sania S. Raza and associates recently (September 2010) reported on the changing nature of
bacterial heart disease. In the past gram negative HACEK bacterial endocarditis was most often
associated with injected drug use. While rare, but often fatal, the major gram negative bacteria
involved were, "
Haemophilus species, Actinobacillus, Cardiobacterium, Eikenella and Kingella." More
Pseudomonas species and the Enterobacteriaceae family were also implicated in Non-
HACEK bacterial heart disease. Gram positive bacteria actually cause about 80% of the heart valve
infections. It was unfortunate but most early studies associated Non-HACEK bacterial heart valves
with injected drug use. About 80% of these cases involved
Pseudomonas and Serratia species.
Besides the gram negative Pseudomonas, recent research show members of the gram negative
Enterobacteriaceae family such as
Citrobacter species, Enterobacter, Escherichia coli, Klebsiella,
Proteus, Providencia, Salmonella and Serratia as causative pathogens. These bacteria caused 30%
of the infections in immune compromised individuals. Raza and assocyates also report that urinary
tract infections were the major pathway to heart infections for elderly patients.

Nafziger, DotMed, reported on a survey released 10/22/2010  by Rush University Medical
Center and the Cook County Department of Public Health on the prevalence of Klebsiella
pneumoniae carbapenemase-producing bacteria in Chicago hospitals. This deadly bacteria is
resistant to virtually all antibiotics, except colistin and tigecycline.  This strain of Klebsiella
pneumoniae first showed up on the East Coast in 1999 and Chicago in 2007. Twenty-six Chicago
hospitals reported Klebsiella pneumoniae carbapenemase-producing bacteria in 2009. The number
of hospitals increased to 37 in 2010. The average number of infected patients per hospital increased
from 4 to 10. Nafziger said it is even worse in New York hospitals where 30% of the hospital patient
laboratory cultures are positive. Natural antibiotic sensitive Klebsiella pneumoniae is a coliform which
generally causes pneumonia, sepsis (i.e., blood and whole-body inflammatory state) and urinary tract

Environmental Protection Agency employs over 17 thousand people with a budget of
$10.020 billion in discretionary budget authority. The focus of the 2011 budget, which started October
1st, is "developing common-sense steps toward clean air, addressing the climate challenge,
protecting our nation’s waters, cleaning up communities and ecosystems, and strengthening EPA’s
scientific and enforcement capabilities." A major part of the funding ($4,896,505,000.00) is for:
Protecting Human Health; Protecting Water Quality; and Enhanced Science and Research. There is
another $1,764,384,000.00 is to be used for: Preserving Land; Restoring Land; as well as Enhancing
Science and Research, because, "Land is one of America’s most valuable resources and cleaning up
our communities to create a safe environment for all Americans is a priority for EPA. Hazardous and
nonhazardous wastes on the land can migrate to the air, groundwater, and surface water,
contaminating drinking water supplies, causing acute illnesses or chronic diseases, and
threaten healthy ecosystems in urban, rural, and suburban areas." "Clean water is essential for our
quality of life and the health of our communities."

It is self-evident with 17 thousand employees, a 10 billion dollar budget and a Congressional mandate
to protect human health that EPA and associated scientist would know all about these studies and
others showing coliforms are disease causing organisms in sludge and water. The only conclusion to
be drawn is that EPA is more interested in transferring liability from industry and municipalities to
farmers and the public at large. EPA's continued claim that coliform bacteria do not cause disease is
a disservice to the public and proof that it has no interest in fulfilling its Congressional mandated
responsibility to protect public health.


1.       A Dictionary of Biology, Coliform,  2004. (October 10, 2010).

2.      Australian Veterans’ Entitlements Act 1986,
Determination of Statement of Principles  
, Instrument No.57 of 1997,

3.     Bowen, Byron D.,  Witebsky, Ernest,
Service of the Buffalo General Hospital,

4.     Borenstein, Jeffrey T,
Acting together, bacterial clusters initiate coagulation, Nature Chemical
Biology 4, 718 - 719 (2008),

5.     Brouqui, P., Raoult, D.,
Endocarditis Due to Rare and Fastidious Bacteria, Clinical Microbiology
Reviews, January 2001, p. 177-207, Vol. 14, No. 1,

6.     Baumgart. Martin, et al.,
Culture independent analysis of ileal mucosa reveals a selective
increasein invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in
Crohn’s disease involving the ileum, The ISME Journal (2007) 1, 403–418, 2007,

7.     Canadian Centre for Occupational Health and Safety,  
Extrinsic Allergic Alveolitis,

8.     Coats, Joseph; Sutherland, Lewis K.,
A Manual Of Pathology, (1900), Longmans, Green, And Co,

9.     COLEMAN, P.N., . TAYLOR, S.,
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The Bacillus Coli Communis, Boston Med Surg J (1894); 131:511-515

11.   Deitch, Edwin A., et al.,
Inhibition of Endotoxin-induced Bacterial Translocation in Mice, J. Clin.
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12.   DE LA Vaissiere, Claude ; Goiffon, Bernard, Corporate Author : ARMY BIOLOGICAL LABS
(Medical Concourse), Vol 85, (1963), PP 185-188,

13.   Diskin, Arthur,
Gastroenteritis, emedicine from WebMD, Oct 22, 2009,

14.   Dorland's Medical Dictionary for Health Consumers,
Coliform, © (2007) by Saunders, an imprint
of Elsevier, Inc.

15.   Dorland, W.A. Newman,
The American Illustrated Medical Dictionary, 1922,  W.B. Saunders
Company, Philadelphia.

16.   Dulaney, Anna Dean; and  Michelson, I. D.,
A Study of B. coli mutabile from an Outbreak of
Diarrhea in the New-born, Am J Public Health Nations Health. 1935 November; 25(11): 1241–

17.   EPA, FY 2011
Budget in Brief,

18.   Es, L. Van,
Colibacillosis, Missouri Valley Veterinary Bulletin, Volumes 5, No 2, Page 55, (1909)

19.   Farrar, W. Edmund JR.; Kent,  Thomas H.;  Ellioit, Van B.,
Lethal Gram-Negative Bacterial
Superinfection in Guinea Pigs Given Bacitracin, JOURNAL OF BACTERIOLOGY, August, 1966,
Vol. 92, No. 2,

FDA, Bacteriological Analytical Manual, Chapter 4, Enumeration of Escherichia coli and the Coliform
Bacteria, http://www.fda.

Epidemiol. (1961) 73 (2): 224-230.

21.   Gay, Clive C.,
Escherichia coli and Neonatal Disease of Calves, BACTERIOLOGICAL REVIEWS,
Mar., 1965, Vol. 29, No. 1,

22.   Humphrey, Isaac P., Kelly, Mirabelle, Gibbs, Barnett, Sinave, Christian P.,
Infections, (2009), E Medicine, WebMD,

23.   Joseph, Tessy A.; Pyati, Suma P.; Jacobs, Norman,  
Neonatal Early-Onset Escherichia coli
Disease, The Effect of Intrapartum Ampicillin, Arch Pediatr Adolesc Med. 1998;152:35-40,

24.   Kaijser, B., Jodal, U.,
Escherichia coli K5 antigen in relation to various infections and in healthy
individuals, J Clin Microbiol 1984; 19:264-6,

25.   Kim, K.J., Elliott, S.J., Di Cello, F., Stins, M.F., Kim K.S.,
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- arteriosclerotic
heart disease
E. coli
Kelbsiella -
EPA would have you believe coliform and fecal coliform are some form of benign
bacteria that indicates there may be fecal contamination or disease causing
microorganisms in food, water or sewage and sewage sludge. It would also have you
believe there is some safe level of these microorganisms. While a good immune
system will protect most people, it is possible to be infected and not know it.  For the
past 116 years medical scientists have been documenting that coliform, now called the
Enterobacteriaceae family, are potential killers of animals and humans. Currently, they
are responsible for approximately 50% of all hospital acquired infections. They can
enter the body through cuts and scraps on the skin,  nose,  mouth, eyes, ears, or
sexual organs. These bacteria also create endotoxins, enterotoxins, and exotoxins
which may be very deadly. The coliform bacterial endotoxins attack the linings of the
stomach and intestines and allow the bacteria to slip through the walls into the blood
where the infection is carried to all major organs. Besides diarrhea, they may cause
brain damage, strokes, heart attacks, aneurysms, blood clots, arthritis, abscesses in
bone joints, cascading organ failure, (kidney, liver, lungs, etc.), shock and death.