Gastrointestinal infections:

Introduction
Salmonella
Escherichia coli
Vibrio
 RESIDENT MICROBIAL FLORA

▰ Human GIT is colonized by diverse group of normal

resident microbial flora.
▰ Upper GIT contains only sparse flora (streptococci
in oral cavity and lactobacilli in stomach).
▰ Lower GIT: The microbial load gradually increases
towards lower part of GIT and is highest in the
distal ileum (1011 to 1012/g). 2
 RESIDENT MICROBIAL FLORA
(Cont..)
▰ The large bowel comprises of both anaerobes and
aerobes with a ratio of 1,000:1; with Bacteroides
fragilis (most common) and Enterobacteriaceae
such as E. coli, Klebsiella present predominantly
▰ Normal flora also comprises of yeasts (e.g.
Candida) and parasites (e.g. Entamoeba coli).
3
PATHOGENESIS OF
GI INFECTIONS
Parasitic infections caused by protozoa and
intestinal helminths are among the most prevalent
Mechanism of disease production by bacteria:
Production of toxins
Invasion and multiplication
• Diarrhea
• Gastroenteritis
• Dysentery
• Food poisoning
• Small intestinal pathology:
Large volume, watery stools (enteritis), without pus
or blood
Diagnosis based on stool examination with the
unaided eye and microscopy
• Large intestinal pathology:
Frequent, small-volume stools with pus and/or
blood
Diagnosis based on stool examination with the
unaided eye and microscopy
 GASTROENTERITIS
Inflammation of stomach and intestines resulting
from bacterial invasion or toxins or viral infection
Manifests with vomiting and diarrhea
 Dysentery
Clinical condition characterised by
 Frequent passage of bloodstained, mucopurulent
stools
The two common types of dysentery are:
(i) Bacillary
(ii) Amoebic
 FOOD POISONING
Acute manifestation of diarrhea (diarrheic type) or
vomiting (emetic type)
Caused by toxins produced by microorganisms
Bacterial toxin-mediated food poisoning: Short
incubation period since the toxins in the food are
preformed
i) Staphylococcus- and Bacillus cereus-related food
poisoning
Incubation period of 1–6 hours
Diarrhea, abdominal cramps, nausea and vomiting
are common symptoms
Transport media for stool
 LABORATORY DIAGNOSIS OF GI INFECTIONS
• Microscopy
Wet preparation: To detect pus cells and RBCs,
and ova, cysts or segments of adult parasites
Saline and iodine preparation: To detect helminth
ova, protozoan cysts and protozoan trophozoites
Concentration techniques: Formol ether or salt
floatation techniques
 LABORATORY DIAGNOSIS OF GI INFECTIONS
Gram-stained smear: Has limited use in the
diagnosis of GI infections
Presence of a large number of yeast cells in an
immunocompromised host or infant
Presence of curved bacilli, suggestive of Vibrio
ZN stain: Modified acid-fast stain
For the identification of coccidian parasites like
Cryptosporidium, Cystoisospora and Cyclospora
Electron microscopy: For the identification of
viruses
 LABORATORY DIAGNOSIS OF GI INFECTIONS
• Culture of faeces
Direct culture:
Non-selective media, e.g., MacConkey agar
Selective media, e.g., xylose lysine- deoxycholate (XLD) agar,
deoxycholate citrate agar (DCA) or thiosulfate-citrate-bile
salt sucrose agar (TCBS) are used
Enrichment culture: To isolate pathogens if their
number is small
Fresh feces are introduced into an enrichment medium like
Selenite F broth, tetrathionate broth (incubated for 12–18
hours) or alkaline peptone water (6–8 hours)
Following this, a subculture is made on the solid culture
medium used for direct plating
 LABORATORY DIAGNOSIS OF GI INFECTIONS
 Isolated organism is identified by biochemical tests and
serotyping
 Antibiotic sensitivity tests: For Shigella, Vibrio and
Salmonella isolates
 Tissue culture: Done for epidemiological or research
purposes only
 Serology: ELISA for the detection of E. coli O157: H7
(EHEC), Shiga toxin and C. difficile toxins
 PCR: To detect Norwalk and other viral agents
 Detection of enterotoxin and Rapid diagnostic tests
(RDT)
 TREATMENT
Acute diarrhea: Fluid and electrolyte replacement
Viral diarrheas (70-80%) are self-limiting and may
require only fluid and electrolyte correction
Infective bacterial diarrheas (cholera) or dysentery
(shigellosis) may require appropriate antibiotics like
ceftriaxone, ciprofloxacin and tetracycline
Parasitic causes: metronidazole and tinidazole may
be used to treat individuals
 CONTRAINDICATION OF ANTIBIOTICS IN GI
INFECTIONS
 They may increase the risk of hemolytic uremic syndrome
in children infected with E. coli O157, H7 (Shiga toxin-
producing E. coli)
 Prolonged use of antibiotics may also lead to the
development of resistance in the normal gut flora in
addition to the pathogen
 Antibiotics suppress the normal flora, allowing C. difficile
or Candida to overgrow, invade and cause necrotising
enterocolitis
 Viral diarrheas (>70%) are NOT to be treated with
antibiotics
 BACTERIAL CAUSES OF
GASTROINTESTINAL INFECTIONS
(ZOONOTIC)
 SALMONELLA (NON-TYPHOIDAL SALMONELLAE)

 Common species:
 S typhimurium (MC)
 S. enteritidis, S. haldar
 S. heidelberg, S. agona
 S. virchow, S. seftenberg
 S. indiana, S. newport and S. anatum
 EPIDEMIOLOGY
Infection via ingestion of contaminated water
and food—mainly poultry (including eggs and
egg products), meat, milk and milk products
Eating salads and undercooked meat and meat
products
Salads and other uncooked vegetables
contaminated by manure or handling
Cross-infection in hospitals
 PATHOGENESIS
Typhoidal or septicemic type of fever
 CLINICAL FEATURES
Incubation period of 24 hours or less
Diarrhea, vomiting, abdominal pain and fever are
the main clinical features
Self-limiting in most cases
Subsides in 2–4 days
In neonates and children  fluid and electrolyte
loss might lead to dehydration and electrolyte
imbalance and may turn fatal unless treated
immediately
 LABORATORY DIAGNOSIS
Feces culture
In outbreaks of food poisoning, culture of the article
of food suspected to have been contaminated also
• TREATMENT
Uncomplicated, non-invasive Salmonella
gastroenteritis: Antibiotics should not be used
Serious, invasive cases: Antibiotic treatment is
needed
• CONTROL
By adhering to personal and food hygiene
 ANTIBIOTIC RESISTANCE IN SALMONELLA
Multidrug resistant salmonellae: By conjugation,
important agents of hospital cross-infections
R factors conferring multiple drug resistance – first
reported in England in the 1960s
These resistant strains have become widely
disseminated among salmonellae
Vaccines do not protect against Salmonella
gastroenteritis or Salmonella septicemia
 ESCHERICHIA COLI
• Gram negative bacilli 1-3x 0.4-0.7µ.
• Arranged singly or in pairs.
• Motile by peritrichous flagella (few strains non-motile).
• Fimbria and capsules are present in some strains.
• Non-sporing.

36
H antigen- Helps in serological diagnosis
 TOXINS

• Two types of exotoxins are produced- haemolysins

and enterotoxins.

• Haemolysins:
• Not relevant in pathogenesis.
• Produced more commonly by virulent strains than
by avirulent strains.

39
• Enterotoxins- Three types.

 Heat labile toxin (LT).

 Heat stable toxin (ST).
 Verotoxin (VT), also called Shiga-like toxin.

HEAT LABILE
TOXIN

40
42
Heat stable toxin
 Assay LT ST

IN VIVO TESTS

Ligated rabbit ileal

loop test
Read at 6hr ± +
Read at 18hr + _

Infant rabbit bowel + +

Infant mouse
intragastric (4hr) _ +

Adult rabbit skin + _

(vascular permeability
factor)
•A1 subunit binds to 28S rRNA- disrupt protein synthesis.
•Destruction of intestinal villus - ↓absorption ,↑fluid
secretion.

Shiga toxin
E coli
 CLINICAL FEATURES
Diarrhea
Septicemia, neonatal sepsis and neonatal meningitis
Urinary tract infection
 Enteropathogenic E. coli (EPEC)
Diarrhea in infants and children and usually produce
institutional outbreaks
O26,O55,O86,O111,O114,O119,O125,O126,O128,O
142.
Non-invasive and do not produce enterotoxins
Plasmid-encoded protein, EPEC adherence factor
(EAF) for adherence
•Adhere to epithelial cells of the small
intestine- destruction of the microvilli.
•Form microcolonies- destruction of
microvilli and diarrhea by malabsorption.
 Enterotoxigenic E. coli (ETEC)
i) Endemic diarrhea in developing tropical countries
Seen in all age groups
From mild, watery diarrhea to a fatal disease
indistinguishable from cholera

ii) Traveller’s diarrhea

 In persons from non-endemic areas
06, 08, 015, 025, 027 and 0167
Adhere to intestinal mucosa by Colonisation Factor

Antigens
ETEC produce enterotoxins which may be either LT or ST
or both
 Enteroinvasive E. coli (EIEC)
Invade interstitial epithelial cells as seen in
shigellosis
Serogroups 028 ac, 0112 ac, 0124, 0136, 0143,
0114, 0152 and 0154
Molecular serotyping of clinical isolates - used to
diagnose EIEC infection
HeLa or HEp-2 cell invasion in culture can also be
used as a diagnostic test
• Pathogenesis:
• Like Shigella species they penetrate the epithelial
cells of the large intestine and multiply intra-
cellularly leading to blood and mucus in stool.
• Spread to neighbouring cells causes inflammation
and tissue destruction, thus leading to bacillary
dysentery.
• Pathogenicity (also Shigella) depends on both
chromosomal and plasmid genes.
• Infections usually food borne (evidence of cross
infection also). 53
• Symptoms range from mild diarrhea to frank
dysentery.
• In children and in adults.
 Acute inflammatory responses.
 Tissue destruction.
 Diarrhea with little fluid, lot of blood & mucous with
polymorphs.

54
 Enterohemorrhagic E. coli (EHEC)
Produce two potent toxins, verocytotoxin (VT) and
Shiga-like toxin (SLT)
Produce fatal hemorrhagic colitis and hemorrhagic
uremic syndrome (HUS)
In young children and the elderly
Primary target - vascular endothelial cells
HUS- characteristic renal lesion is capillary
microangiopathy
• Hemorrhagic colitis:
• IP- 1-5 days.
• Manifests- watery
diarrhea to severe
hemorrhagic colitis.
• Accompanied by
abdominal cramps
and vomiting.

56
• Diarrhea becomes bloody in 1-2 days, usually not
associated with fecal leucocytes.
• Fever seen in a third of the cases.
• Infection lasts for 4-10 days.
• E coli O157:H7 & O26:H11 are the common strains.
• Low infective dose ~ 10-100 bacilli sufficient to
spread the infection from one child to another by
fecal-oral route.

57
58
 Enteroaggregative E coli (EAggEC)
• They show typical stacked brick arrangement on
HEp-2 cells or glass due to autoagglutination.
• Bundle forming fimbriae (AAF/I, AAF/II), carried on a
plasmid, mediate this process.

60
• EAEC strains secrete a low molecular weight heat-
stable enterotoxin called enteroaggregative heat
stable enterotoxin-1 (EAST-1).
• EAEC increases mucus secretion, forming a layer
over the epithelium.
• This biofilm traps the bacteria in the epithelium of
the small intestine.

61
• In animal experiments they cause shortening of
microvilli, mononuclear infiltration and
hemorrhages.
• Persistent mucous, watery diarrhea.
• Vomiting and dehydration in infants.

62
 Diffusely adherent E coli (DAEC)
• DAEC- watery diarrhea primarily in children (1-5yr).
• Identified by their ability to adhere to culture cells.
• They cause elongation of the microvilli, with
bacteria being trapped in the cell membrane.

63
64
 Prevention & Treatment
Antibiotic treatment is not indicated for E. coli
diarrhea
Personal hygiene and food safety for prevention
No vaccines available
VIBRIO

67
• Second major group of Gram negative, facultatively
anaerobic, fermentative bacilli.
• The group has three genera:
1. Vibrio- Vibrionaceae.
2. Aeromonas- Aeromonadaceae.
3. Plesiomonas- closely related to Proteus, now has
been placed in Enterobacteriaceae.

• All of them are considered together because of

similarities in epidemiology and range of diseases,
in spite of taxonomic reorganization.
68
• The genus grossly is divided into:
1. Nonhalophilic vibrios- includes Vi cholerae and
other species which are able to grow on media
without added salt.
2. Halophilic vibrios- require the presence of added
salt in their growth media.

69
 Vibrio cholerae
• Morphology:
• Gram negative, short curved, cylindrical rods, 1.5µ x
0.2-0.4µ with rounded or slightly pointed ends.
• Cell is typically comma shaped (old name Vi
comma), but curvature is lost on subcultures.
• Pleomorphism is frequent in old cultures.

70
 GARDENER
&
VENKATARAMAN
1935
73
 Vibrio cholerae O139
• Cases caused by these organisms were reported in
1992 from Chennai (indistinguishable from O1).
• Similar outbreaks followed in different parts of
India.
• By mid January 1993 similar isolates were found in
Bangladesh, and spread to all over north along the
course of major rivers.
• This new strain, not agglutinable with O1 antiserum,
was called O139 Bengal.

77
• Pathogenesis:
• Natural infection occurs only in humans.
• Vibrios enter orally via contaminated water and
food (feco-oral transmission).
• Infective dose 108 bacilli.
• Achlorhydria predisposes.
• Any medication or condition reducing the stomach
acidity predispose.

78
Exotoxin

79
 Cholera
• It is an acute diarrheal disease.
• Incubation period varies from <24hr to 5 days.
• Clinical illness begins with mild diarrhea and
vomiting in 1-3 days or abruptly with sudden
massive diarrhea.
• 60% are of the classical Vi cholerae cases.
• 75% of El Tor vibrio cases are asymptomatic.

80
• In the severe forms it presents as profuse painless
watery diarrhea, with copious effortless vomiting
leading to hypovolemic shock and death in <24hr.
• In treated cases the disease lasts for 4-6 days, during
which period the patient passes a total volume of
liquid stool equal to twice his body weight.
• All the clinical features are due to massive loss of
fluid and electrolytes.

81
82
83
• Cholera stool:
• It is typically colorless watery fluid with flecks of
mucus, said to resemble water in which rice has
been washed (rice watery stool).
• It has characteristic inoffensive sweetish odor.
• It is bicarbonate-rich isotonic, electrolyte solution
with little protein.

84
• It’s outpouring leads to diminution of ECF volume,
hemoconcentration, hypokalemia, base-deficit
acidosis and shock.
• Rapid loss of fluid and electrolytes, leading to
profound dehydration, circulatory collapse & anuria.

85
• Complications:
• Muscular cramps, renal failure, pulmonary edema,
arrhythmias, paralytic ileus.
• Mortality without treatment- 25 to 50%.
• El Tor vibrios cause milder disease.

86
91
• LAB DIAGNOSIS
• Stool specimens should be collected fresh, before
antibiotic intake.
• Specimen is best collected by insertion of a
lubricated catheter into the rectum, and let the
liquid stool flow directly into a screw capped
container.
• Rectal swabs made of good quality cotton wool can
be used, absorbing 0.1-0.2ml of fluid.
• Useful in collecting specimens from convalescents.

93
• The swabs should be moistened with transport
medium before sampling (in a plastic bag if no
transport medium available).
• Collection from the bed pan not encouraged (risk of
contamination & disinfectants).
• Vomitus is not useful.

94
• Transport:
• Specimens should be preserved at 40C or in a
holding medium like VR medium or Cary-Blair
medium (die within a few hr).
• Specimens should reach immediately to the lab, if
delay of >6hr, in an enrichment medium- APW or
Monsur’s medium.

95
• 1-3ml of feces to 10-20ml of transport medium.
• This saves time required for isolation.
• If transport media are not available, strips of
blotting paper may be soaked in the liquid stool and
sent in plastic envelopes.
• If possible, specimens should be plated at the bed
side.

96
• Microscopy:
• If the stool reaches within 15-30 min after passage,
darting motility can be demonstrated using a
hanging drop preparation (dark field or phase
contrast microscope preferred).
• In the dark field, vibrios evoke the image of many
shooting stars in a dark sky.
• The sample can be mixed with group O1 and O139
antiserum and immobilization observed in dark field
microscopy.

97
• Simple test still practiced- distilled water
immobilization test.
• A Gram stain is not very conclusive.
• Direct immunofluorescence has been attempted,
but non specific background fluorescence is
common.

98
• Culture:
• The samples should be plated both directly and
after enrichment on to suitable solid media.
• The enrichment media should be held for 6-8 hr
(including transit time) before plating.
• Specimens received in holding media are put in to
enrichment media (6-8 hr), then plated.

99
• Media usually employed are bile salt agar,
MacConkey agar (non-selective), and TCBS agar,
GTTA agar (selective).
• Plates should not be older than 3-5 days, should be
dried well.
• Gram stain- Gram negative curved rods.
• Oxidase and motility tests.

100
Hi chrome vibrio agar

101

Fig. 24.8 String test used to
differentiate Vibrio spp. From
Aeromonas spp. and Plesiomonas
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LABORATORY
DIAGNOSIS
Identification: Vibrio colonies
identified by performing the
‘string test’ in 0.5% sodium
deoxycholate saline on a slide.
A ‘string’ is formed by DNA
material that is released from the
vibrios as a result of the lysis of
the cells by sodium deoxycholate
Serogrouping: Agglutination
with cholera O subgroup
• Slide agglutination:
• Oxidase positive vibrio suspect colonies should be
picked up for slide agglutination with O1 antiserum.
• If positive, agglutination repeated with specific
Ogawa and Inaba antisera.
• Hikojima strains will agglutinate with both Ogawa
and Inaba antisera.
• If negative with one colony, repeat with at least
another five colonies as O1 & non-O1 isolates may
co-exist in the same specimen.

103
104
• If slide agglutination is positive, the isolate is further
tested with biochemicals for differentiation
between El Tor and classical vibrios.
• A report can be sent at this stage (2nd day after
specimen received).
• The disease has to be notified up to WHO.
• If no vibrios are isolated, a 2nd cycle of enrichment
and plating may succeed.

105
106
• The isolates not agglutinable with O1 antiserum
should not be ignored, as non O1 vibrios are known
to produce cholera-like disease.
• An antiserum to H antigen, shared by all cholera
vibrios can be used.
• Vibrio agglutinated with H antiserum, not by O1
antiserum is considered to be non-O1 cholera vibrio.
• Specific antiserum against O-139 is available.

107
• Biochemical reactions:
• Use of O/F test, Moeller’s arginine dihydrolase, lysine
and ornithine decarboxylase, arabinose, inositol,
mannose, sucrose sugar fermentation tests, test for
growth in the absence of sodium chloride (1%
tryptone water) or CLED agar plate.

• The strain may be sent to International Reference

Center for vibrio phage typing- National Institute of
Cholera and Enteric Disease (NICED) at Kolkata.

108
• Serological diagnosis:
• Not very useful.
• Paired serum samples can be tried in previously non
immunized persons.
• Antibody to cholera toxin can be detected by ELISA
• Serological examination is of little value, may be to
assess the prevalence of cholera.
• Agglutination with live or killed vibrio suspensions,
IHA, vibriocidal test, antitoxin assay.
• Of these, Complement dependent vibriocidal
antibody test is the most helpful.
109
110
• Detection of carriers:
• The same techniques are used, except for more
than one cycle of enrichment is needed.
• Vibrio excretion is intermittent, so repeat stool
sampling should be done.
• Examination of stool after a purgative (mannitol 30
gm or magnesium sulphate 15-30gm).
• For bile, after intubation.

111
• Examination of water samples:
• Enrichment or filtration methods may be employed.
• Enrichment method:
• 900ml of water is added to 100ml of ten fold
concentrated peptone water at pH 9.2, incubated at
370C for 6-8hr, and a second enrichment done
before plating on selective media.

112
• Filtration method:
• The water to be tested should be filtered through a
millipore membrane filter, which is then placed
directly over a selective medium and incubated.

• Sewage should be diluted in saline, filtered through

gauze and treated as water.

113
115
 PREVENTION
i) Parenteral vaccines: Killed suspensions of V.
cholerae—as subcutaneous or intramuscular injection
ii) Oral vaccines
1. Killed oral whole cell vaccines
2. Live oral vaccines with classical, El Tor and O-139
strains, with their toxin genes deleted
Two doses of the vaccines are required for full
protection (minimum 1 week and maximum 6 weeks
apart)
Three doses are required for children aged 2–5 years
(minimum 1 week and maximum 6 weeks apart)
 TREATMENT

Adequate replacement of fluids and

electrolytes using oral rehydration
solution (ORS)
Antibacterial therapy
 Doxycycline is recommended as the first-line treatment for
adults
 azithromycin is recommended as first-line treatment for
children and pregnant women

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 VIBRIO MIMICUS

 Infection acquired by eating seafood, especially oysters

 The disease is self-limiting
 Clinical manifestations resemble those caused by V.
parahaemolyticus

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 HALOPHILIC VIBRIOS

Vibrios that have a high requirement of sodium chloride

Their natural habitats are seawater and marine life

Halophilic vibrios known to cause human disease

• V. parahaemolyticus
• V. alginolyticus
• V. vulnificus

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 Resembles the cholera vibrio except that it is capsulated and shows bipolar
staining
 Produces peritrichous flagella when grown on solid media and polar flagella in
liquid cultures
 Grows only in media containing NaCl; tolerates salt concentrations up to 8%
 On TCBS agar, the colonies are green; string test is positive
 Differentiated from V. cholerae by various biochemical reactions
 Three antigenic components have been recognised—somatic O, capsular K and
flagellar H antigens
 Kanagawa phenomenon: Hemolysis in special high-salt blood agar (Wagatsuma
agar)
 Only the Kanagawa positive strains are pathogenic

VIBRIO PARAHAEMOLYTICUS
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PATHOGENESIS
 V. parahaemolyticus causes food poisoning associated with
marine food
 Acute diarrhea and enteritis
 Wound infections, sepsis are rare

TREATMENT
 Infection is usually self-limiting
 In severe cases of gastroenteritis, doxycycline is the antibiotic
of choice
 Uncomplicated wound infections, minocycline or doxycycline
may be used

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 VIBRIO ALGINOLYTICUS

 Resembles V. parahaemolyticus
 Associated with infections of the eyes, ears and
wounds in human beings exposed to seawater

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 VIBRIO VULNIFICUS

VP-negative and ferments lactose but not

sucrose
Salt tolerance of less than 8%
It causes two types of illnesses:
1. Wound infection following contact of open wounds with seawater
2. septicemia with high mortality: In immunocompromised hosts,
particularly those with liver disease
 Following the ingestion of the vibrio, usually in oysters
 Does not cause gastrointestinal manifestations; it enters the
bloodstream

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 AEROMONAS AND
PLESIOMONAS
 Rarely associated with diarrhea
 Aeromonas hydrophila: Causes diarrhea
and some pyogenic wound infections in
humans
 Plesiomonas shigelloides: Causes
diarrheal disease
 Both these are oxidase-positive, polar
flagellated, gram-negative rods and may
be mistaken for vibrios
 They may be differentiated from vibrios
by biochemical tests such as utilisation of
amino acids

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This Photo by Unknown Author is licensed under CC BY-NC-ND
 ANTIGENIC STRUCTURE
• Serotyping based on 3 antigens:
 Somatic O antigen.
 Flagellar H antigen.
 Capsular K antigen

• Detectable in agglutination assays with specific

rabbit antibodies.
• Antigenic pattern of a strain given as the number of
particular antigen it carries- O111:K58:H2
127
• Somatic O antigen
• Heat stable (resistant to boiling for 2½ hr), LPS of
the cell wall.
• > 170 types identified (1,2,3 etc).
• Cross react with O antigens of other members of
Enterobacteriaceae.
• Normal colon strains belong to early O groups
(1,2,3,4 etc), enteropathogenic strains belong to
later O groups (26,55,86,111 etc).
• Typing done by slide agglutination (if K is present
cultures have to be boiled).
128
• Flagellar H antigen
• Heat and alcohol labile proteins present on flagella.
• Genus specific, usually not shared (with other
Enterobacteriaceae).
• 75 H antigens recognized so far.
• Better expressed in semisolid media.

129
• Capsular K antigen
• Acidic polysaccharide antigen located in the
envelope or microcapsule (K ~ Kapsel, German for
capsule).
• Encloses the O antigen and renders the strain
inagglutinable with O antisera.
• May also contribute to virulence by inhibiting
phagocytosis.
• Poor activators of Complement.
• 103 K antigens recognized so far.

130
• K antigens are of two types- I & II.
• E coli K I antigen shows cross reactions with
Neisseria meningitidis and Haemophilus influenzae
capsular antigens.
Properties Group I Group II
Molecular weight >100000 Da <50000 Da
O GROUPS O8,O9 Many
Acidic component Hexuronic Glucuronic acid, phosphate,
acid KDO, Neu-NAc
Electrophoretic Low High
mobility
Expressed at 17-200C Yes No
Chromosome site His Ser A
Susceptibility to Heat stable Heat labile
heat at 1000C 131
• Fimbrial F antigens
• On fimbria, heat labile proteins (heating at 1000C).
• No role in antigenic classification.
 Common fimbriae (chromosomally mediated,
mannose-sensitive hemagglutination)- not relevant
in pathogenesis.
 Plasmid coded, in small numbers, mannose
resistant hemagglutination- act as virulence factors.
• Some occur only as surface antigens (not
morphologically separate).
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 VIRULENCE FACTORS

• Two types- surface antigens and toxins.

• Surface antigens:
• Somatic O antigen:
• Endotoxic activity, protects against phagocytosis
and C effects.
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• Fimbriae:
• For initial attachment and colonization.
• K88 & K99 antigens important in causing diarrhea in
animals.
• Colonization Factor Antigens (CFA) in human diarrhea.
• In UTIs- P fimbria binds specifically to P blood group
substance on human erythrocytes and uroepithelial
cells- uropathogenic strains.

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