Escherichia coli

(E. coli)

WRITTEN REPORT
 Escherichia coli (E. coli)

INTRODUCTION

Escherichia coli is one of the predominant facultative anaerobes in the human

gastrointestinal tract. It was first described by Theodor Escherich in 1885 as
Bacterium coli commune when he isolated it from the feces of newborns. Later on, it
was renamed Escherichia coli; for many years, the bacterium was simply considered
to be a commensal organism of the large intestine. It was not until 1935 that a
strain of E. coli was shown to be the cause of an outbreak of diarrhea among
infants. [1]. Many strains of E. coli are harmless and even provide many health
benefits to the host, including preventing colonization of the gut by harmful
pathogens. However, there are small groups of E. coli that have evolved and
developed pathogenic strategies that can cause a broad spectrum of disease, including
several diarrheal disease and serious sequelae, in the human host and are more
commonly referred to as pathogenic E. coli. These virulence attributes are frequently
encoded on genetic elements that can be mobilized into different strains to create
novel combinations of virulence factors, or on genetic elements that might once have
been mobile, but have now evolved to become ‘locked’ into the genome. Only the
most successful combinations of virulence factors have persisted to become
specific ‘PATHOTYPES’ of E. coli that are capable of causing disease in healthy
individuals. Three general clinical syndromes can result from infection with one of
these pathotypes: enteric/diarrhoeal disease, urinary tract infections (UTIs) and
sepsis/meningitis. Among the intestinal pathogens there are six well-described
categories: enteropathogenic E. coli (EPEC), enterohaemorrhagic E. coli
(EHEC), enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC),
enteroinvasive E. coli (EIEC) and diffusely adherent E. coli (DAEC). UTIs are the
most common extraintestinal E. coli infections and are caused by uropathogenic E.
coli (UPEC). EPEC, EHEC and ETEC can also cause disease in animals using many
of the same virulence factors that are present in human strains and unique
colonization factors that are not found in human strains. The various pathotypes of E.
coli tend to be clonal groups that are characterized by shared O
(lipopolysaccharide, LPS) and H (flagellar) antigens that define SEROGROUPS
(O antigen only) or SEROTYPES (O and H antigens)2,4. Pathogenic E. coli
strains use a multi-step scheme of pathogenesis that is similar to that used by other
mucosal pathogens, which consists of colonization of a mucosal site, evasion of
host defences, multiplication and host damage. Most of the pathogenic E. coli
strains remain extracellular, but EIEC is a true intracellular pathogen that is
capable of invading and replicating within epithelial cells and macrophages.
Pathogenic E. coli strains possess specific adherence factors that allow them to
colonize sites that E. coli does not normally inhabit, such as the small intestine and
the urethra. Most frequently, these adhesins form distinct morphological structures
called fimbriae (also called pili) or fibrillae, which can belong to one of several
different classes. Fimbriae are rod-like structures of 5–10 nm diameter that are
distinct from flagella. Fibrillae are 2–4 nm in diameter, and are either long and wiry
or curly and flexible.

ETEC causes watery diarrhoea, which can range from mild, self-limiting
disease to severe purging disease. The organism is an important cause of childhood
diarrhoea in the developing world and is the main cause of diarrhoea in travellers to
developing countries. ETEC colonizes the surface of the small bowel mucosa and
elaborates enterotoxins, which give rise to intestinal secretion. Colonization is
mediated by one or more proteinaceous fimbrial or fibrillar colonization factors (CFs),
which are designated by CFA (colonization factor antigen), CS (coli surface antigen)
or PCF (putative colonization factor) followed by a number.

EIEC are biochemically, genetically and pathogenically closely related to

Shigella spp. The four Shigella species that are responsible for human disease, S.
dysenteriae, S. flexneri, Shigella sonnei and Shigella boydii, cause varying
degrees of dysentery, which is characterized by fever, abdominal cramps and
diarrhoea containing blood and mucous. EIEC might cause an invasive
inflammatory colitis, and occasionally dysentery, but in most cases EIEC elicits
watery diarrhoea that is indistinguishable from that due to infection by other E.
coli pathogens. EIEC are distinguished from Shigella by a few minor biochemical
tests, but these pathotypes share essential virulence factors. EIEC infection is thought
to represent an inflammatory colitis, although many patients seem to manifest
secretory, small bowel syndrome. The early phase of EIEC/Shigella pathogenesis
comprises epithelial cell penetration, followed by lysis of the endocytic vacuole,
intracellular multiplication, directional movement through the cytoplasm and
extension into adjacent epithelial cells.

I. DEFINITION OF THE DISEASE

The diarrheal disease caused by ETEC is characterized by a rapid onset of

watery, non-bloody diarrhea of considerable volume, accompanied by little or no
fever. Escherichia coli diarrheal disease is contracted orally by ingestion of food or
water contaminated with a pathogenic strain shed by an infected person. The
disease requires colonization and elaboration of one or more enterotoxins. Both
traits are plasmid-encoded. ETEC diarrhea occurs in all age groups, but mortality is
most common in infants, particularly in the most undernourished or
malnourished infants in developing nations. Infection with ETEC is the leading
cause of travelers' diarrhea and a major cause of diarrheal disease in lower-income
countries.

Enteroinvasive E. coli (EIEC) may produce an illness known as bacillary

dysentery. The EIEC strains responsible for this syndrome are closely related
to Shigella spp. Following the ingestion of EIEC, the organisms invade the
epithelial cells of the intestine, resulting in a mild form of dysentery, often
mistaken for dysentery caused by Shigella species. The illness is characterized by
the appearance of blood and mucus in the stools of infected individuals.
Dysentery caused by EIEC usually occurs within 12 to 72 hours following the
ingestion of contaminated food.

II. SYNONYM
Enterotoxigenic Escherichia coli
Enteroinvasive Eschirichia coli
Traveller’s Disease
Gastroenteritis

III. MORPHOLOGICAL DESCRIPTION OF THE BIOLOGICAL AGENT

© http://www.microbiologyinpictures.com/escherichia%20coli.html

As for its morphological description, Escherichia coli (E. coli) a unicellular

organism, is the head of the Enterobacteriaceae (enteric bacteria) which are anaerobic
Gram-negative bacteria that commonly reside in the intestinal tracts, especially lower
intestine, of warm-blooded organisms (endotherms). It is one of the most important
bacteria in the medical industry. E. coli can respond to environmental signals such as
chemicals, pH, temperature, osmolarity, etc., For example, it can sense the presence or
absence of chemicals and gases in its environment and swim towards or away from
them. Or it can stop swimming and grow fimbriae that will specifically attach it to a cell
or surface receptor.

ETEC: has a pili (colonization factor) also called as fimbriae (also called pili) or
fibrillae which can belong to one of several different classes. These are rod-like
structures of 5–10 nm diameters that are distinct from flagella. Fibrillae are 2–4 nm in
diameter, and are either long and wiry or curly and flexible. The pili helps it bind to
intestinal epithelial cells, where it releases exotoxins which are similar to the cholera
exotoxins.

EIEC: has a main virulence factor encoded in a plasmid shared by E. Coli and
Shigella ; the plasmid gives the bacteria the ability to invade the epithelial cells.

Pictured above are (R) Unstained cells of E. coli viewed by phase microscopy
with about 1000X magnification (©CDC) and (L) four different strains of Escherichia
coli on Endo agar. Another feature of E. coli is being a “lactose fermenter”– those that
consume lactose or other six-carbon sugars and metabolize them through the process
of lactic acid fermentation. This process of fermentation releases the energy contained
within the bond of the sugars and produces the byproduct lactic acid. [4]. In addition,
Colonies of some strains have typical greenish metallic sheen but many of them grow
without it. It is from the Eosin Methylene Blue media that assists in visual distinction
(as color indicator) for Escherichia coli, other nonpathogenic lactose-fermenting
enteric gram-negative rods, and the Salmonella and Shigella genera [5].

Most E. coli strains are harmless, but some may cause serious food poisoning in
humans. The bacterium is versatile and well-adaptive to its habitat. It can grow in
media with glucose as the sole organic constituent. Wild-type E. coli has no growth
factor requirements, and metabolically it can transform glucose into all of the
macromolecular components that make up the cell. E. coli can grow in the presence or
absence of O2. Under anaerobic (intestinal) conditions it will grow by means of
fermentation, producing characteristic "mixed acids and gas" as end products.
However, it can also grow by means of anaerobic (extra-intestinal) respiration, since it
is able to utilize NO3, NO2 or fumarate as final electron acceptors for respiratory
electron transport processes [1].

IV. CLINICAL HORIZON (SIGNS & SYMPTOMS)

 Symptoms ETEC infections include diarrhea without fever. The bacteria
colonize the GI tract by means of a fimbrial adhesin, e.g. CFA I and CFA II, and
are non-invasive, but produce either the LT or ST toxin. Other common symptoms
are abdominal pain, malaise, nausea, and vomiting. Diarrhea and other symptoms
cease spontaneously after 24 to 72 hours. Infection with ETEC can cause profuse
watery diarrhea and abdominal cramping. Illness develops 1-3 days after
exposure. Some infections may take a week or longer to resolve. Symptoms rarely
last more than 3 weeks. Most patients recover with supportive measures alone and
do not require hospitalization or antibiotics.

The illness caused by EIEC is characterized by abdominal cramps, diarrhea,

vomiting, fever, chills, and a generalized malaise. Dysentery caused by this
organism is generally self-limiting with no known complications. A common
sequelus associated with infection, especially in pediatric cases, is hemolytic
uremic syndrome (HUS). Patients with E coli dysentery (caused by enteroinvasive E
coli [EIEC] or enterohemorrhagic E coli [EHEC]) have fever, bloody diarrhea, and
dehydration. Intestinal mucosa produces a significant inflammatory response.
Clinically, patients with E coli dysentery present with fever and have blood and PMN
leukocytes in their stool. The differential diagnoses of E coli dysentery
include shigellosis and amebic dysentery.

V. INCUBATION PERIOD
The incubation period of ETEC and EIEC diarrhea are usually 3 to 4 days,
although incubation times as long as 5 to 8 days or as short as 1 to 2 days have been
described in some outbreaks. The initial complaint is usually nonbloody diarrhea,
although this is preceded by crampy abdominal pain and a short-lived fever in many
patients. Vomiting occurs in about half of the patients during the period of nonbloody
diarrhea and/or at other times in the illness. Within 1 or 2 days, the diarrhea becomes
bloody and the patient experiences increased abdominal pain. This stage usually lasts
between 4 and 10 days. In severe cases, fecal specimens are described as “all blood
and no stool”. In most patients, the bloody diarrhea will resolve without apparent
sequelae, but in about 10% of patients younger than 10 years (and in many elderly
patients), the illness will progress to HUS.

VI. PERIOD OF COMMUNICABILITIES

A person can spread E. coli during the acute illness and can shed E. coli in stool
for up to 3 weeks after symptoms resolve [6]. E. coli outbreaks are usually the
result of widespread food contamination.
VII. LABORATORY DIAGNOSIS

There are many causes of diarrhea. Stool cultures and other tests should be
obtained to eliminate the more common causes of diarrhea such as:

 Campylobacter
 Salmonella
 Shigella
 E.coli 0157:H7
 Viruses

Specific laboratory tests for ETEC are not widely available at commercial
laboratories. Specialized laboratories including those at the Centers for Disease
Control and Prevention are able to identify this organism. Serotyping and tests for
virulence factors are occasionally performed for outbreaks.

The culturing of the organism from the stools of infected individuals and the
demonstration of invasiveness of isolates in tissue culture or in a suitable animal
model is necessary to diagnose dysentery caused by this organism. More recently,
genetic probes for the invasiveness genes of both EIEC and Shigella spp. have been
developed.

All patients with suspected E coli infection should undergo routine CBC count
with differential to evaluate for leukocytosis or a left shift. Gram stain results
determine if the organism is gram-negative, but findings do not distinguish among
the other aerobic gram-negative bacilli that cause similar infectious diseases. E coli is
a gram-negative bacillus that grows well on commonly used media. It is
lactose-fermenting and beta-hemolytic on blood agar. Most E coli strains are
non-pigmented. Definitive diagnosis is based on the isolation of the organism in the
microbiology laboratory from clinical specimens. Specimens may be blood, urine,
sputum, or other fluids such as cerebrospinal, biliary, abscess, and peritoneal.
Recovery of the organism in contaminated sites, such as sputum and wounds, must be
analyzed in the context of the patient's clinical state to determine if it represents
colonization or infection. Recovery from sterile sites, such as the CSF, should be
considered diagnostic of infection.
VIII. TREATMENT

Clear liquids are recommended for persons with diarrhea to prevent dehydration
and loss of electrolytes. For adults, packaged oral rehydration salts or premixed oral
rehydration solutions (both available over-the-counter) may be used, although
traditional remedies with salty liquids such as chicken soup are also effective.
Bismuth subsalicylate compounds can help reduce the number of bowel movements.
Although antimotility agents can effectively relieve ETEC-associated diarrhea and
cramps, they may prolong the time it takes the body to rid itself of the toxin.
Antimotility medications should be avoided by persons with high fevers or bloody
diarrhea, and should be discontinued if diarrhea symptoms persist more than 48 hours.
There are no data showing that kaolin-pectin compounds or lactobacillus slows
diarrhea or relieves abdominal cramping.
Antibiotics can shorten the duration of diarrheal illness and discomfort, especially if
given early, but they are usually not required. ETEC and EIEC are frequently resistant
to common antibiotics, including trimethoprim-sulfamethoxazole and ampicillin.
Because resistance to antibiotics is increasing worldwide, the decision to use an
antibiotic should be carefully weighed against the severity of illness and the risk of
adverse reactions, such as rash, antibiotic-associated colitis, and vaginal yeast
infection. Fluoroquinolones, Penicillins, Amino-glycosides and 2nd and 3rd gen.
cephalosporins have been shown to be effective therapy.

IX. PROGNOSIS

ETEC and EIEC are both usually a short, self-limiting illness lasting on
average 3-5 days. (However, EIEC at times fall under poor prognosis when found
in HIV patients.) The illness may present either as (1) acute watery diarrhea, (2)
diarrhea with blood (dysentery) or (3) chronic diarrhea, often with clinical
evidence of fat or carbohydrate malabsorption. The majority of cases are due to
intestinal infection and resolve without specific treatment. Antibiotics can reduce
the severity and duration of the illness and are always indicated for dysenteric
shigellosis and amoebiasis. Oral rehydration therapy is the mainstay for managing
water and electrolyte depletion [8]. The prognosis worsens with the development of
complications. Good hydration lessens the chances of complications and improves the
outcome, thereby creating it excellent [7].

X. PREVENTION/CONTROL MEASURES
ETEC

Prevention depends on sanitary measures to prevent fecal-oral transmission;

hand-washing and proper preparation of food; chlorination of water supplies; and
sewage treatment and disposal. Parenteral or oral fluid and electrolyte replacement is
used to prevent dehydration. Broad-spectrum antibiotics are used in chronic or
life-threatening cases. Escherichia coli diarrheal disease is best controlled by
preventing transmission and by stressing the importance of breast-feeding of infants,
especially where ETEC is endemic.

The primary control strategy for ETEC is prevention of oral-fecal transmission

through building sanitation infrastructure. Other measures can be taken to control
infection, these include cooking food and keeping it hot, peeling fruits and vegetables,
and using water that has been boiled or chemically treated with iodine, chlorine, or
another disinfectant. Secondary to prevention, management of the disease using oral
rehydration therapy reduces morbidity and mortality associated with the disease.

EIEC

Prevention and control are generally the same as for ETEC. Intervention of the
fecal-oral transmission cycle is most effective in institutional situations.
Broad-spectrum antibiotics are recommended in chronic and/or life-threatening cases.

REFERENCES:
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Calderon, M.D.
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[5]
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