Transcript Slide 2 from last year with the additional info from this year sheet

Note that there are a lot of information in the
sheet are not included here, also there are a
lot of information mentioned in the slides are
not in the sheet, what is colored in red is
from the sheet, I did my best to clarify these
slides, enjoy.
There are 6 groups of E. coli strains which have
virulence factors causing human diarrhea..Widely
distributed in water, and the intestine of animals
& Birds and human
 .there are.4 most important types
1-Enterotoxigenic E. coli (ETEC). Common in
domestic animals, Poultry, Humans .it. Produces
Heat stable (ST) or Heat -labile enterotoxins (
LT).. (plasmid borne) or both
it is attached to enterocytes of the small
intestine’s epithelium by fimbrial adhesins
attachment
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LT subunit B.. Similar to Cholera toxin,
attached to GM1 Ganglioside, releases
subunit A which activates adenylyl cyclase &
increases cellular cAMP release .
Heat-stable toxin (ST) activates cGMP.. Both
cause prolonged hyper secretion of water &
sodium + chloride ions which Inhibits
reabsorption of sodium.. Mild/severe watery
diarrhea, vomiting, abdominal pain.. No fever.
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ETEC strains are frquent & important cause of
diarrhea in infants/very young children &
common cause of Traveler’s diarrhea in
developed countries.
Contaminated water, Dairy products, fresh
vegetable food.
Self- limited with oral rehydration, Antibiotics
are rarely needed, develop intestinal immunity.
2- Entero-haemorrhagic E. coli (EHEC) Which are
associated with the release of toxins known as
Shiga-like toxin / Vero-toxigen.. There are many
serotypes associated with this organism, but the
most important one is O157: H7. in relation to
somatic Ag and O Ag. ,
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common in intestines of animals/ cows.. and
it transmitted to human by close contact or
contamination of meats especially raw meats
like Hamburger , also contamination of milk
& ground beef meat.. causes outbreaks of
gastroenteritis & later Haemolytic Uraemic
Syndrome (HUS).
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Complications: Severe inflammation & ulceration
colon, Bloody-purulent diarrhea Haemorrhagic
colitis.. If toxin reached blood & reach Kidneys
results HUS (HUS).. More severe in children/old
patients.. Release Blood+ Protein in urine.. Kidney
failure highly fatal.
Prevention is better than treatment with
antimicrobials.
3-Entero-pathogenic E.coli (EPEC).. K, Related to
lipopolysaccharides LPS Antigens adherence to GI
epithelium & distortion.. numerous serotypes.. often
produce diarrhea in neonates up to age 6 months.
Outbreaks watery diarrhea & vomiting in infant
nurseries aged less 6 months.. Normally produce
mild diarrhea but may associated with chronic
diarrhea and death of the child
.
4-Entero-invasive E.coli (EIEC).. Similar to 
Shigella causes bloody diarrhea due to
ulceration in large intestine ,Vomiting,
Abdominal pain, Fever.. by invasion of
damaging intestinal epithelial cells..
necrosis.. Affect all ages..more common and
severe in children
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Detection of Diarrheagenic E. coli strains in the
laboratory is difficult.. complicated by the fact
that non-virulent E. coli strains are commonly
present in the feces.
Stool culture on MaConkey agar and other type
of agar can't easily distinguish between
pathogenic and not pathogenic ones.
Identification by PCR more accurate than
biochemical and serotyping.
4-Entero-invasive E.coli (EIEC).. Similar to
Shigella causes bloody diarrhea due to
ulceration in large intestine ,Vomiting,
Abdominal pain, Fever.. by invasion of damaging
intestinal epithelial cells.. necrosis.. Affect all
ages..more common and severe in children
4-Entero-invasive E.coli (EIEC).. Similar to 
Shigella causes bloody diarrhea due to
ulceration in large intestine ,Vomiting,
Abdominal pain, Fever.. by invasion of
damaging intestinal epithelial cells..
necrosis.. Affect all ages..more common and
severe in children
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Campylobacter spp. are Microaerophlic, Gramnegative,Spiral shape.. Bipolar flagella.. Motile..
microaerophilic bacteria, not easily identified in
normal culture media, it needs special antibiotic
type media  campylobacter media.
Commonly present in the GIT of domestic animals..
poultry & pets .. Contaminate easily Meat, Dairy
products, fresh Food & Direct contact with
animals.. Common cause of diarrhea in Western
countries..Less in Arab countries. Depending on
species of campylobacter, there’re many types of
the diarrhea
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Campylobacter jejuni: Release Endotoxin &
various enterotoxin/cytotoxins.. Acute
enteritis, Watery Diarrhea and rarely bloody
diarrhea(in the slides is says bloody diarea
but the sheet says it rarely cause it) , few
days, Infants, children > adults, Elderly. Rare
septicemia, Reactive arthritis followed chronic
diarrhea.
Infection is mostly self-limited without
treatment. Prolong carriage associated with
immunodeficiency.
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Campylobacter fetus.. Less common human
diarrhea( in the sheet it says more common)..
Commonly causes sepsis & abortion in
animals. Culture is more significant then
serological test in diagnosis clinical chronic
cases.
Treatment: Macrolides/Azithromycin,
Ciprofloxacin, Ampicillin (Normally, under
health condition, no need to give antibiotic
drugs, only control dehydration, if necessary
replacing by oral tube without any
complication.)
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This is the only organism which has many
association with the mucosa of our
gastrointestinal specially stomach mainly gastric
antrum.
Microaerophlic growth.. Gram-ve spiral shape,
motile, polar 4-6 flagella .. produces potent
urease, neutralize stomach acidity, allow
colonizing mucus overlaying gastric mucosa
mainly gastric antrum.
H. pylori colonize stomach of 30%-90% of
world’s population according their age.. Mostly
without signs or symptoms and may not cause
any disease.
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Pathogenicity: Protease, outer membrane
antigens & Cytotoxins causing chronic
inflammation of the inner lining of the
stomach mucosa.. Gastritis, Peptic /dudenal
ulcers. , first mild unrecognized later increase
in about .about 2 % infected persons.
H. pylori discovered 1983 as cause of
chronic gastritis.. Complications Gastric
lymphoma, Stomach cancer in infected
persons over a long period.
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Infection is most likely acquired by ingesting
food, water, personal/family contact. Reinfection is common. Optimal growth..selective
culture medium with 90% Co2 , 42 C, 3-5 days.
More acidity cause more ulceration.
Diagnoses: A) clinically by Urea breath test ,
using urea capsule labeled with active carbon
detects urease activity in stomach by splitting
urea into Co2 & Ammonia. B) A rapid urease test
for identification H. pylori in gastric biopsy
taken by endoscope or culture
Giemsa /silver stain by histological examination.
Serological antibodies test is less significant.
Treatment : there are 2-3 antibiotics should given
together , like metronidazole and clarithromycin and
anti-acids , this combination should be continued at
least 4 weeks , eradicated is not 100%.
It’s only for short period. Patient will recurrent this
infection.
Infection is not easily controlled without controlling the
stress condition. or Metronidazole + Amoxicillin + H2 Blockers..
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Vibrio group is Gram-negative straight or curved
rods, oxidase-positive, motile, single polar
flagellum.. Most types are found Commonly in sea
water-human cycle. There are 20 species, 2 main
types are
Classical V. cholerae (- in relation to presence of
somatic Ag 01), 0139 El-tor type.. Infect only
human.. Cause Epidemic/Pandemic responsible for
at least in each year 1,000,000 cases of cholera
disease.Outbreaks.. Spread from India
subcontinent.
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Noninvasive.. affecting small intestine
through Heat-labile Cholera Toxin (A and B
subunits) B-unit binds to Gangliosies release
A-unit.. , same mechanism as enterotoxins
heat labile toxin of E.coli; Increasing cAMP
causing outpouring large amount water, Na+,
K+ Cl- , HCO- ..
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Incubation period . 8-24h..Severe watery
diarrhea (1-3 Liters) ,vomiting & cramps,
rapid dehydration(which can be within few
hours and might end body fluids in less than
result in complication, cardiac arrest - kidney
failure - death.), shock, blood acidosis, renal
failure.. death within 24 h if patient not
received replacement of fluid loss .
Partial intestinal immunity.. antitoxin
antibodies last for 1-year, Oral vaccine is
effective for short period.
Non-01 V. cholerae.. found in water along with
0-1 V.cholerae Less virulent.. watery diarrhea
similar to classical cholera due to release
cytotoxins not so severe .
 It’s more cytotoxic  affect mucosa of large
intestines.
 V. parahaemolyticus.. Halophilic Vibrio..
Cytotoxins
Raw fish. Gastroenteritis.. May cause Sepsis or
Wound infection.. Contaminated row fish
* Lab Diagnosis: Stool culture.. Special culture
TCBS ((4 components: Thiosulfate-citrate-bile
salts-sucrose medium )
),
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Biochemical & serotyping confirmation with
specific cholera antisera to differentiate
different subtypes.
* Treatment: Oral rehydration is the main
treatment.. Replacement of fluid
loss..doxycycline, cotrimoxazole (children),
ciprofloxacin reduce the Vibrios excretion
* Prevention: you should have Safe water &
Food.. Early detection of positive infected
cases prevent outbreak of cholera in
community.. No Healthy carriers.
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Food poisoning organisms , are not important
only in presence of bacteria in intestinal tract ,
it’s more important in release of toxins in already
presented food , which means if there is
contamination of food particles with these types
of bacteria , you should expect that these
organisms will release potent toxins 
responsible for food poisoning or what we called
food intoxication .
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Staphylococcus aureus strains associated
with specific bacteriophage types can
produce several Heat-stable protein
exotoxins in food ( 20 minutes 100C), Fast
absorbed from small Intestine to Blood
stream & affects CNS. Staphylococcal food
poisoning is commonly associated with salty
foods, cream cakes, grounded meat.. Fresh
dairy products.. White chesses.
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Main Symptoms: 30 minutes-6 hours
following the consumption of the
contaminated food.. vomiting, nausea,
stomach cramps.. rarely watery diarrhea.. No
fever & recovery within 1-2 days.. Selflimited.
Diagnoses: detection of Staph. toxins in eaten
food.
Bacillus cereus.. G+ve Aerobic Spore-Forming Bacilli,
Common in Nature.. Spores survive boiling and
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cooling/refrigeration Food.. Produces 2 types of
toxins, exotoxins/ enterotoxins produced during
bacilli sporulation either in Food or Intestine..
Associated with two main gastrointestinal symptoms.
1-Intoxication .. Heat-Acid stable Emetic
Enterotoxins .. Typically developed within 1-24
hours of eating contaminated fried rice, meat..
Vomiting nausea, stomach cramps last for few hours
without diarrhea & fever. 2- Diarrheal Toxins/
HL..watery mild diarrhea.. No Fever or
Vomiting..self-limiting within 1-3 days.
Both Types of toxins may produce from the same B.
cereus strain.. Mostly outbreaks in family, schools &
commonly associated with Chinese food.. Fried rice
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Anaerobic, spore-forming Gram+ve, Part of normal intestinal
flora of neonates & infants.. Adults (5-20%).. Rapidly increased
colonization in hospitalized patients & become active danger
after antibiotic treatment for more than 1 week.. with all widespectrum peniciilins, clindamycin cephalosporins.. Often
causes nosocomial infection among elderly, surgery &
compromised patients.
Antibiotic-associated enterocolitis developed by release
2 toxins types (enterotoxin A, cytotoxin B) acting directly on
intestinal epithelial cells causing necrosis.. Bloody diarrhea..
Increased rapidly within days to severe Pseudomembranous
colitis.. Another new strain producing more potent binary
toxin detected few years ago. Treatment: stop use potential
causative antibiotics, use metronidazole / vancomycin will
prevent disease complication.
Done by Mohanned Momani, dedicated to
mamoon and ameen kajjon
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