Part 503 list -1989
                                        This list was removed from the final 1993 Part 503

EPA Office of Water is fully aware of the multitude of deadly disease organism in sludge - biosolids products.
But EPA and its partners still claim it is safe at 1 million coliform per kilo for Class A and 2 billion for Class B?


Occurrence of Pathogens in Distribution and Marketing Municipal Sludges (1988)
EPA Pathogen list from Part 503 (1989)


For the most part, EPA was less than truthful when it listed the diseases caused by these bacteria in sludge.
It would have been impossible to claim biosolids was safe if the list had been left in the sludge guidelines.


1.    Campylobacter jejuni -------------------------   Gastroenteritis.

Campylobacter is considered by many to be the leading cause of enteric illness in the United States (20,26).
Campylobacter species can cause mild to severe diarrhea, with loose, watery stools often followed by bloody diarrhea.
Campylobacter species are highly infective. The infective dose of C. jejuni ranges from 500 to 10,000 cells, depending
on the strain, damage to cells from environmental stresses, and the susceptibility of the host. The infections are
manifested as meningitis, pneumonia, miscarriage, and a severe form of Guillain-Barré syndrome.  Environmental
stresses, such as exposure to air, drying, low pH, heating, freezing, and prolonged storage, damage cells and hinder
recovery to a greater degree than for most bacteria. Older and stressed organisms gradually become coccoidal and
increasingly difficult to culture.

Diarrhea (may be bloody), fever, abdominal pain, and cramps,
bloodstream infection (bacteremia) may lead to infections of other organs, joints may becomes painful, red, and swollen;
abdominal pain; and enlargement of the liver or spleen. The infection may involve the heart valves (endocarditis) or the
tissues covering the brain and spinal cord (meningitis). (Merck)

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

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)

3.     Salmonella sp ------------------------------------ Gastroenteritis and enteric fever.

2,200 strains, Each type can produce gastrointestinal upset, enteric fever, and specific localized infections, nausea and
cramping abdominal pain, watery diarrhea, fever, vomiting, spread through bloodstream to infect other sites, such as
the bones (particularly in people with sickle cell disease), joints, or heart valves (Merck)

Typhoid fever (enteric fever) is caused by Salmonella typhi . Typhoid bacteria enter the digestive tract and gain access
to the bloodstream. Inflammation of the small and large intestine follows. In severe infections, which can be life
threatening, sores may develop in the small intestine. These sores bleed and sometimes perforate the intestinal wall.
loss of appetite, fever, headache, joint pain, sore throat, constipation (or, less commonly, diarrhea), and abdominal pain
and tenderness. A brassy, nonproductive cough is common. Nosebleed may occur. fever remains high, and the person
may become delirious, slow heartbeat and extreme exhaustion, intestinal bleeding or perforation occurs,  Pneumonia
may develop, Infection of the gallbladder and liver also may occur. A blood infection (bacteremia) occasionally leads to
infection of bones (osteomyelitis), heart valves (endocarditis), kidneys (glomerulitis), the genitourinary tract, or the
tissues covering the brain and spinal cord (meningitis). Infection of muscles may lead to abscesses (collections of pus).

4.     Shigella sp ----------------------------------------- Gastroenteritis.

The genus Shigella consists of four species: S. dysenteriae (subgroup A), S. flexneri (subgroup B), S. boydii (subgroup
C), and S. sonnei (subgroup D). Shigella organisms may be very difficult to distinguish biochemically from Escherichia
coli. Brenner (1) considers Shigella organisms and E. coli to be a single species, based on DNA homology.

cause disease by penetrating the lining of the intestine—primarily, the large intestine—resulting in swelling and
sometimes shallow sores, abdominal pain and watery diarrhea,  develop seizures, eye inflammation and reactive arthritis
(Reiter's syndrome), intestinal perforation may occur, part of the rectum to be pushed out of the body, Permanent loss
of bowel control can result, Weight loss and dehydration may become severe and leads to shock and death. (Merck)

5.     Vibrio Cholerae -------------------------------------Cholera

V. cholerae (6), the type species of the genus Vibrio, is the causative agent of cholera outbreaks and epidemics.
Cholera enterotoxin (CT) is the primary virulence factor of the disease cholera. A Florida study of illnesses from raw
shellfish consumption reported the following species in descending order of frequency; V. parahaemolyticus, non-
O1/O139 V. cholerae, V. vulnificus, V. hollisae, V. fluvialis, O1 V. cholerae (64,72).
in 1993, a large outbreak of cholera occurred in India/Bangladesh from a new, until then unknown serogroup, O139.
The O139 strain has become endemic in the Bengal region and is the cause of what may be known as the Eighth
Cholera Pandemic. Some non-O1/O139 strains also are invasive, produce a heat stable toxin, and have caused septic
infections in individuals with pre-disposing medical conditions. V. vulnificus (33), the leading cause of death in the US
related to seafood consumption and nearly always associated with raw Gulf Coast oysters (90,104), resembles V.
parahaemolyticus on TCBS agar, but can be differentiated by several biochemical reactions, including -galactosidase
activity (31). Epidemiological and clinical investigations have shown that V. vulnificus causes septicemia and death
following ingestion of seafood or after wound infections originating from the marine environment

Food supplies may be contaminated by the use of human feces as fertilizer or by freshening vegetables for market with
contaminated water. A number of common-source gastroenteritis outbreaks attributed to V. parahaemolyticus have
occurred in the US (57), associated with oyster consumption.  The invasive species, V. vulnificus, the causative agent of
septicemic shock (63,90,118), is a common organism in coastal waters of some areas of the US and other countries
(60,90,122,124). It is reported to cause 20 to 40 U.S. cases each year of primary septicemia with a 50% mortality rate
among individuals with liver disease and elevated serum iron levels (104). A review of cases has determined an
association between septicemia and consumption of raw oysters, nearly all from Gulf Coast waters. This species has
also been responsible for wound infections in individuals who are associated with marine environments.  http://www.

painless, watery diarrhea and vomiting, severe dehydration, with intense thirst, muscle cramps, weakness, and minimal
urine production, may lead to kidney failure, shock, coma, and death. (Merck)


(Yanko, 1988) Yesinia - streptococci - toxigenic E. coli - Leptospira spp - enterotoxigenic, enteropathogenic and

the genus Yersinia has grown to include eleven species (2,8,9,50), three of which are potentially pathogenic to humans:
Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica
The association of human illness with consumption of Y. enterocolitica-contaminated food, animal wastes, and
unchlorinated water is well documented (4,5). Refrigerated foods are potential vehicles. because contamination is
possible at the manufacturing site (4) or in the home (5). This organism may survive and grow during refrigerated
Some strains of Y. enterocolitica and related species produce an in vitro heat-stable enterotoxin (ST). Virulent strains of
Yersinia invade mammalian cells such as HeLa cells in tissue culture (29). However, strains that have lost other virulent
properties retain HeLa invasiveness, because the invasive phenotype for mammalian cells is encoded by chromosomal
loci. Transfer of these genetic loci into E. coli confers the invasive phenotype to the E. coli host. all virulent Y.
enterocolitica isolates were shown to be tissue culture-invasive and to carry the ail gene.  http://www.cfsan.fda.

The presence of a large number of S. aureus organisms in a food may indicate poor handling or sanitation; however, it
is not sufficient evidence to incriminate a food as the cause of food poisoning. The isolated S. aureus must be shown to
produce enterotoxins. Conversely, small staphylococcal populations at the time of testing may be remnants of large
populations that produced enterotoxins in sufficient quantity to cause food poisoning.  Processed foods may contain
relatively small numbers of debilitated viable cells, whose presence must be demonstrated by appropriate means.
Analysis of food for S. aureus may lead to legal action against the party or parties responsible for a contaminated food.
In all cases, the reactions of enterotoxigenic and nonenterotoxigenic strains varied by 12% or less. This research
indicates that none of these tests can be relied upon to differentiate toxic and nontoxic staphylococci. http://www.cfsan.

Among the metabolites produced by Staphylococcus aureus, and other staphylo-coccal spp., enterotoxins (5,16,27)
present the greatest foodborne risk to the health of consumers. Staphylococcal enterotoxins are basic proteins
produced by certain Staphylococcus strains in a variety of environments, including food substrates. These structurally-
related, toxicologically similar proteins are produced primarily by Staphylococcus aureus, although S. intermedius and S.
hyicus also have been shown to be enterotoxaemia. When large numbers of enterotoxigenic staphylococci grow in
foods, they may elaborate enough toxin to cause food poisoning after the foods are ingested. The most common
symptoms of staphylococcal food poisoning, which usually begin 2-6 h after contaminated food is consumed, are
nausea, vomiting, acute prostration, and abdominal cramps.

The presence of small numbers of C. perfringens is not uncommon in raw meats, poultry, dehydrated soups and
sauces, raw vegetables, and spices. Because the spores of some strains are resistant to temperatures as high as 100°
C for more than l h, their presence in foods may be unavoidable. Furthermore, the oxygen level may be sufficiently
reduced during cooking to permit growth of the clostridia. Spores that survive cooking may germinate and grow rapidly
in foods that are inadequately refrigerated after cooking.

The symptoms, which include intense abdominal cramps, gas, and diarrhea (nausea and vomiting are rare), have been
attributed to a protein enterotoxin produced during sporulation of the organism in the intestine. The enterotoxin can be
detected in sporulating cultures, and a method for this purpose is included. A high correlation has been established
between the ability of C. perfringens strains to produce enterotoxin and their ability to cause food poisoning. However, it
is difficult to obtain consistent sporulation with some strains. C. perfringens cells lose their viability when foods are
frozen or held under prolonged refrigeration unless special precautions are taken. Such losses may make it difficult to
establish C. perfringens as the specific cause of a food poisoning outbreak.