Morphology and virulence factors of

helicobacter pylori
Background
Spiral shaped organisms occasionally visualized in gastric mucosa layer, but
no evidence of disease was found

Organism was first classified as Campylobacter pylori

Marshall and Warren cultured organism from human gastric mucosa and
showed association with gastritis and peptic ulcer disease for which they won
Nobel Prize in 2005
 MORPHOLOGY OF H.pylori
 Helicobacter pylori is spiral shaped.
 It is a gram negative bacilli.
 It has lophotrichous flagella ( tuft of 5 to 7 flagella)
 Flagella gives corkscrew motility.
 Size: 0.5-1.0 * 2.5-5.0 µm.
 It is non-spore forming and non-capsulated.
 Cell wall is composed of lipopolysaccharides.
 On surface , urease enzyme is present.
 Found in acidic pH of 2 or less.
 It is microaerophilic (5-15%)
 -Spiral shaped ( 0.5-1.0*2.5-5.0 µm)
-Non capsulated
-Non spore forming

-Lipopolysaccharides (cell wall) -Lophotrichous Flagella

-Urease enzyme in surface -Tuft of 5 to 7 Flagella
-CORKSCREW motility
Gram negative Rods

Warthin-Starry Stain
shows black-rod shaped H.pylori
Cork screw motility
Virulence factors
1. Urease
2. Flagella
3. Mucinase
4. Cytotoxin-associated gene A (CagA)
5. Vacuolating Cytotoxin A (VacA)
6. Blood group antigen-binding adhesin
7. Outer inflammatory protein A
8. Duodenal ulcer promoting gene A
 1.Urease

• Protects from the

gastric acidity
due to the
increased release
of ammonia.
• The enzymatic
reaction of
urease is based
on the hydrolysis
of urea

Modulates the host immune responses (facilitated apoptosis, chemotaxis of neutrophils and monocytes, altered
opsonization, enhanced release of the pro-inflammatory cytokines)
 2. Flagella

• Enhances bacterial
motility
• Stimulates chemotaxis
• Facilitates inflammation
and immune evasion.
 3.Mucinase

• It helps to breakdown mucin layer that is present between

epithelial lining of stomach and hydrochloric acid.
• It reduces mucous viscosity and facilitate bacterial
movement.
4. Blood group antigen-binding adhesin(Bab-A)

- Enables bacterial adherence to gastric epithelial cells

- Stimulates the delivery of toxins (due to the increased Type 4 secretion

system (T4SS) activity)

- Stimulates the inflammatory responses (excessive IL-8 release,

granulocyte infiltration)
 5. Cytotoxin-associated gene A
(CagA)
• Stimulates inflammatory
responses
• Induces the release of IL-8 and IL-
12
• It triggers reorganization of actin
skeleton within the intoxicated
cell.
• CagA protein is the leading factor
for the oncogenic protein and
thus is responsible for CagA
Adenocarcinoma of stomach.
 6. Vacuolating Cytotoxin A (VacA)

• Involved in the formation of pores

• Promotes the autophagy pathways ,forms
the intracellular vacuoles. VacA
• Induces apoptosis of epithelial cells
• Inhibits the activity and proliferation of T
and B cells (Immune cells)
T4SS
 7. Outer inflammatory protein A

• Activates the apoptotic cascade

• Promotes the secretion of the pro-inflammatory
cytokines such as IL-1, IL-6, IL-8, metalloproteinase.
• Regulates β-catenin levels (β-catenin have key role
in cell proliferation, differentiation and
apoptosis)
 8. Duodenal ulcer promoting gene A

• Involved in the formation of T4SS

• Stimulates the infiltration of the inflammatory cells
• Facilitates urease and IL-8 secretion and IL-12 release from
the monocytes
• Activates the mitochondria-mediated apoptotic pathways
• Facilitates bacterial tolerance in the acidic
microenvironment
.
.
REFERENCES:
• ESSENTIAL OF MEDICAL MICROBIOLOGY –APURBA S SASTRY, SANDHYA BHAT

• Ananthanarayan and Paniker’s TEXTBOOK OF MICROBIOLOGY

•An Overview Of Bacterial Virulence Factors And Pathogenesis- BIOMEDICAL JOURNAL

 PBL – GROUP E Members :
1. ALANKRIT NARAYAN
2. ARPANA NEPAL
3. MANOJ NEUPANE
4. ARPAN NIRAULA
5. ABHIRAJ PAJIYAR
6. DIPESH PAUDEL
7. SONIYA RAI
8. ASHUTOSH RAJ
9. AARATI RAUNIYAR
10. SANDEEP RAUNIYAR
11. AMRIT RIJAL
12. SHWETA ROY
13. BIBEK SAH
14. DEEPA SAH
THANKS TO:

• Dr. Ritu Baral

• Dr. Jyoti Kayastha ( mentor)
• Dr. Kewal Shrestha ( faculty microbiology)