DIARRHOEA
 Although E-coli is normally carried in the gut
as a normal commensal, it may cause
gastrointestinal disease ranging in severity
from mild self limiting diarrhoea to
hemorrhagic colitis.
 Such strains fall into 5 groups associated with
specific serotypes.
 The major groups of diarrhoea causing E-
coli
Pathogenic group
Common serogroups
Enteropathogenic
E-coli(EPEC)
O26,O55,O86,O111 etc
Enterotoxigenic
E-coli(ETEC)
O6,O8,O15,O25,O27,O167
Enteroinvasive
E-coli(EIEC)
O28,O112,O124,O136,O143,O1
52,O154
Verocytotoxin
producing E-coli
(VTEC)
O26,O157
Enteroaggregative
E-coli (EAEC)
O-untypable
ENTEROPATHOGENIC E-COLI (EPEC)
 They cause infantile diarrhoea usually
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occuring as institutional outbreaks.
They can also cause sporadic diarrhoea in
children and very rarely in adults.
Spread is through oral contamination.
In infantile enteritis there is colonisation of
upper part of small intestine.
In areas of EPEC attachment brush border
microvilli are lost.
 It adheres to the gut wall and causes subsequent
mucosal damage.
 This lesion has been termed as attachment and
effacement lesion.
 Such strains have been termed as AEEC
(attaching and effacing E-coli).
 Pathogenicity is mainly due to the production of
an adhesin ‘intimin’.
 EPEC also synthesize intimin receptors which is
inserted into the gut wall providing binding site
for intimin.
LABORATORY DIAGNOSIS OF EPEC:
Sample collected-stool
Plated on Mac Conkey agar
Pink colonies obtained
Bacteria are examined by slide agglutination with
polyvalent antisera
If positive then identified with monovalent
antisera to individual serogroups.
ENTEROTOXINEGIC E-COLI (ETEC)
 Responsible for community acquired
diarrhoeal disease in areas of poor sanitation
and mainly traveller’s diarrhoea.
 Spread is through ware contaminated by
human/animal faeces.
 These strains produce heat labile (LT) or heat
stable(ST) toxin or both.
 Toxin production itself is not sufficient to
produce diarrhoea.the organism must bind to
the intestinal epithelium.
 This binding is mediated by fimbria that bind to
specific receptors in the intestinal cell
membrane.
 These adhesins have been termed as
colonisation factor antigens(CFAs).
 The first CFA to be recognised was K88.loss of
K88 plasmid was accompanied by loss of
capacity to cause diarrhoea in piglets.
 LABORATORY DIAGNOSIS OF ETEC:
 This is mainly by demonstration of toxins
 LT: Tissue culture with mouse adrenal cells (Y1),chinese
hamster cells(CHO) and vero cells.if toxin is present
in culture it has a cytotonic effect on these cells i.e
producing changes in cell morphology.
 Others:- ELISA,RIA, Biken test (precipitin test).
 ST: Distinguished from LT by its relative stability to heat
and by rapidity of action.
 .
 Widely used method is infant mouse test
 since it is poorly immunogenic initially
immunologic tests were not performed
 Now the toxin is coupled with a hapten (bovine
serum albumin carrier), and the antiserum is
used in RIA.
 ELISA-monoclonal antibodies specific for ST are
done.
ENTEROINVASIVE E-COLI (EIEC)
 Causes disease resembling Shigella dysentry in
individuals of all ages.
 Spread mainly through ingestion of
contaminated food.
 A small no. of bacteria is enough to cause
infection since it is resistant to acid and bile.
 They enter the large intestine and multiply in the
lumen.
 Here they attach to the intestinal epithelial cells
and are endocytosed.
 They cause lysis of the vacuole multiply within the
cell and kill it.
 They then spread to the neighbouring cells, cause
tissue destruction.
 This produces consequent inflammation which is
the underlying cause of the symptoms of bacillary
dysentry.
 Invasiveness of the bacteria is due to an ‘outer
membrane protein’ coded by a large plasmid.
 The plasmid also codes for the ability for the ability
to escape from the endocytic vacuole.
 These strains show ‘O’ antigen cross reactivity with
shigella dysentry.
LABORATORY DIAGNOSIS OF EIEC
 Sereny test
 Tissue culture:- whereby monolayers of Hep-2
cells and Hela cells are exposed to suspensions
of the culture.after an appropriate infection
period the cells are washed with gentamycin and
lysozyme to wash off extra cellular
organisms.the cells are then observed for
intracellular organisms.
VEROCYTOTOXIGENIC E-COLI (VTEC)
 They cause symptoms ranging from mild watery
diarrhoea to severe diarrhoea with large
amounts of blood in the stool (hemorrhagic
colitis) &hemorrhagic uraemic syndrome
(important complication especially in children).
 Disease may occur sporadically or through
outbreaks of food poisoning.
 These strains produce a toxin i.e verotoxin/shiga
like toxin that is cytotoxic to vero cells.
 Since it causes hemorrhagic colitis it is also known
as enterohemorrhagic E-coli.
 In hemorrhagic colitis initially abdominal pain is
seen, followed by watery diarrhoea and finally
bloody diarrhoea usually not associated with fever.
 HUS is characterised by acute renal failure (major
cause of renal failure in children),micro-angiopathic
hemolytic anaemia and thrombocytopenia.
 Vascular endothelial cells are the primary targret for
the toxin.
 It is usually associated with bloody diarrhoea.
 LABORATORY DIAGNOSIS OF VTEC
 DNA probes for the genes encoding VT1
and VT2has been developed.
 PCR with VT-specific primers has also
been used to detect VTEC.
 O157 VTEC strains ferment sorbitol
slowly this property is used for their
identification on sorbitol Mac Conkey
agar. The strains are incubated over
night and then tested with O157 LPS
specific antiserum in a simple
agglutination assay.
ENTERO-AGGRGATIVE E-COLI (EAEC)
 Responsible for chronic diarrhoeal disease in
certain developing countries.
 They are characterised by their ability to adhere
to particular laboratory-cultured cells such as
Hep-2 in an aggregative or stacked brick
pattern.
 Most of them are O untypable but many are H
typable.
 The mechanism by which these strains cause
diarrhoeal illness are poorly understood.
LABORATORY DIAGNOSIS OF EAEC
 The only methods currently available for
detecting these bacteria are the Hep-2 cell
test for determining the aggregative
phenotype and DNA probes.
 The Hep-2 cell test involves allowing strains
of E-coli to adhere to cell monolayers in vitro
and observing the pattern of adhesion by
microscopy.
PYOGENIC INFECTIONS
 Most common cause of intra abdominal
infections that result from spillage of the bowel
contents.
 These include:
peritonitis
perianal infections
abscesses
neonatal meningitis.
SEPTICEMIA
 E-coli may invade into the blood stream and
lead to fatal conditions like septic shock and
systemic inflammatory response syndrome.
PREVENTION AND TREATMENT
 GENERAL MEASURES:
1. Early correction of fluid and electrolye imbalance
to prevent death in severe infections.
2. Avoid exposure to infecting agent.
3. Provision of safe water supplies
4. Education on hygienic practice in the handling
and production of food.
5. Observing strict hygiene in hospitals to prevent
spread of infantile enteritis.
6. Any infected patients should be isolated to
prevent fecal spread.
 ANTIMICROBIAL PROPHYLAXIS:1. Some drugs reduce the incidence of
diarrhoea in travellers to tropical
areas:
 Doxycycline
 Trimethoprim
 Norfloxacin and other
fluoroquinolones.
 However he widespread use of
antibiotic prophlaxis may lead to
drug toxicity and drug resistence.
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