Bacteria that caused

infection in Tr. GI non

diarheae
Pratami Adityaningsari
Bag. Mikrobiologi
FK UY

Bacterial GE can affect one person/a

group of pople who all ate the same food
picnics, school cafetarias, restaurants,
etc.
The m.o get into the food in different
ways :
Meat that contact with m.o from the
intestines of an animal being
processed.
Water that is used cooking may
contain animal/ human waste.

Food poisoning occurs from eating/drinking :

Any food prepared by s.o who didnt wash their
hands properly.
Any food prepared using unclean cooking
utensils, cutting board & other tools.
Dairy product containing mayonnaise that have
been out of the refrigerator too long.
Frozen/refrigerated foods that arent stored at
the proper temperature.
Raw fish/oyster.
Raw fruit/vegetables that have been washed
well.
Undercooked meats/eggs.
Water that hasnt been treated.

Some bacterias that can caused GE :

Campylobacter jejuni
E. coli
Salmonella
Shigella
Staphylococcus
Yersinia
Vibrio
Clostridium
Bacillus cereus
Helicobacter pylori
etc

HELICOBACTER PYLORI
Background
Human stomach long considered inhospitable for
bacteria
Spiral shaped organisms occasionally visualized in
gastric mucous layer, but no evidence of disease
association
Organism classified first as Campylobacter pylori
Now Helicobacter pylori
Other species of Helicobacter isolated from
stomach, intestine of other animals
Marshall and Warren culture organism from human
gastric mucosa and show association with gastric
inflammation

A silver stain of H. pylori on gastric mucus-secreting

epithelial cells (x1000). From Dr. Marshall's stomach
biopsy taken 8 days after he drank a culture of H.
pylori (1985).

MICROBIOLOGY
1. Gram negative, spiral, flagellated
(motile) bacilli
2. Slow growing, requires complex
media, microaerophilic
3. Oxidase and catalase positive
4. Produces urease
5. Noninvasive; proliferates in
mucus overlying gastric type
mucosa
6. Not cleared by host immune
response

TRANSMISSION
1. Humans are major - if not only - reservoir
2. Transmission believed to be by fecal-oral
route
organism can be cultured from feces
family members often carry same strain
prevalence of infection likely related to
inferior hygienic conditions and poor
sanitation
infection from environment or from animals
cannot be totally excluded

EPIDEMIOLOGY
1. Gastric colonization rate in developing countries is
about 80%
Very high from early childhood
2. Gastric colonization rate in US and other
developed countries is about 30%
3. Prevalence of infection increases with age
Age 10 = ~5%
Age 30 = ~ 25%
Age 60 = ~ 50%
4. In US, prevalence rates are higher in AfricanAmericans and Hispanics
5. Age and low income = main risk factors for H.
pylori infection

Evidence supporting H. pylori as major cause

of peptic ulcer disease
1. H. pylori is found in almost all cases of PUD, when
the use of NSAIDs is definitely excluded
2. When H. pylori is treated and eradicated, the rate
of ulcer recurrence is dramatically reduced
3. H. pylori induced changes in acid secretion and
mucosal resistance provide a plausible
pathophysiologic explanation

PATHOGENESIS
Colonization
1. Most bacteria killed in hostile environment of gastric
lumen
2. H. pylori proliferates in mucus layer over epithelium
and is not cleared by host immune response
3. H. pylori survives and grows there because of a
variety of virulence factors that contribute to gastric
inflammation, alter gastric acid production, and cause
tissue destruction.

VIRULENCE FACTORS
Initial colonization facilitated by:
Acid inhibitory protein - blocks acid
secretion from parietal cells during acute
infection
Urease - neutralizes gastric acids due to
ammonia production, also stimulates
monocytes and neutrophil chemotaxis,
stimulates production of inflammatory
cytokines
Heat shock protein - enhances urease
expression; co-expressed with urease on
bacterial surface

 Flagella - allows penetration into

gastric mucous layer
Adhesins - mediate binding to host
cells
Localized tissue damage mediated by:
Mucinases and phospholipases - disrupt
gastric mucus
Vacuolating cytotoxin - induces
vacuolation in epithelial cells that results
in epithelial cell damage

 All these factors plus LPS stimulate

inflammatory response
SOD and catalase - prevent from
phagocytosis and intracellular killing
Plus other poorly defined factors that
stimulate IL-8 secretion by epithelial cells,
that induce nitric oxide synthase which
mediates tissue injury, and that induce
programmed death of gastric epithelial cells.
Cag pathogenicity island - includes genes
that confer enhanced pathogenicity, in part
by inducing epithelial cells to produce
proinflammatory cytokines

Diagnostic Testing for Helicobacter pylori

Endoscopic Testing
1. Histology
Advantages : Excellent sensitivity and specificity
Disadvantages : Expensive and requires infrastructure and trained
personnel
2. Rapid urease testing
Advantages : Inexpensive and provides rapid results.
Disadvantages : Excellent specificity and very good sensitivity in properly
selected patients, Sensitivity significantly reduced in the posttreatment
setting
3. Culture
Advantages : Excellent specificity. Allows determination of antibiotic
sensitivities
Disadvantages : Expensive, difficult to perform, and not widely available.
Only marginal sensitivity
4. Polymerase chain reaction
Advantages : Excellent sensitivity and specificity. Allows determination of
antibiotic sensitivities
Disadvantages : Methodology not standardized acrosslaboratories and
not widely available

 Nonendoscopic Testing
1. Antibody testing (quantitative and qualitative)
Advantages : Inexpensive, widely available, very good NPV
PPV dependent upon background H. pylori prevalence.
Disadvantages : Not recommended after H. pylori therapy

2. Urea breath tests (13C and 14 C)

Advantages : Identifies active H. pylori infection, Useful before
and afterH. pylori therapy
Disadvantages : inconsistent

3. Fecal antigen test

Advantages : Identifies active H. pylori infection. Excellent
positive and negative predictive values, Useful before and
after H.pylori therapy
Disadvantages : Polyclonal test less well validated than the
UBT
in the posttreatment setting. Unpleasantness associated with
collecting stool