H. Pylori is commonly transmitted in childhood in crowded, poor living conditions through oral-oral or fecal-oral routes. It persists by mimicking human glycans to avoid immune responses. Around half the world is infected, with higher prevalence in developing regions. It colonizes the stomach using urease and vacuolating cytotoxin A (VacA) and CagA pathogenicity island virulence factors. Acute infection causes diarrhea and slowed growth while chronic infection leads to gastritis in most cases. H. Pylori is associated with diseases like gastric ulcers and cancer.

1. H. Pylori
Transmission
 Persistence
 Clinical outcome

By,
Bharati Singh

2. Source of infection of H. pylori
Crowded
living condition
Poor living condition
Large family size
Lack of hot running water
Route of transmission
Most H. pylori transmission occur in childhood
Gastric- oral
Oral-oral
Fecal-oral


3. World wide prevalence of Helicobacter pylori

It is estimated that half of the world’s population is infected
with H.pylori.

Infection prevalence shows large geographical variations.
Infection is highly prevalent in Africa, Asia and South America
Bauer et al. (2011) Hindawi publishing corporation, Germany

4. Prevalence of H. pylori infection by age in developed
and developing countries
Logan et al. (2001) BMJ clinical review, 323

5. Colonization of the mucous layer

Capable of colonizing the harsh environment of
the human stomach.

generates substantial amounts of cytosolic and cell
surface associated urease.

uses several other urease independent strategies
to minimise exposure to the low pH in the gastric
lumen.

6. Two major Virulence factors
1. Vacuolating cytotoxin A (Vac A)
2. Cag (cytotoxin associated gene) pathogenicity
island

VacA is an oligomeric toxin, structure resembles “flowers” in
which a central ring is surrounded by peripheral plates.

.
Three reported effects:
• VacA’s effect on endosomal maturation leading to
vacuolation of epithelial cells.
•
Induces host cell death through apoptosis.
•
Cause leakage of ions and small molecules such as
iron, nickel, sugar, amino acid.

7. Cag pathogenicity island and
cagA

encodes the cytotoxin associated gene (cag) pathogenicity
island which expresses a type IV secretion system.

forms a syringe- like pilus structure for the injection of
virulence factor into host target cell.

after delivery, CagA become phosphorylated by tyrosine
kinase and mimics a host cell factor .

8. Stomach mucosa colonized by Helicobacter Pylori
Montecucco et al. (2001) Nat Rev Mol Cell Biol 2, 457-466

9. Persistance


To colonize the human stomach for extended
periods of time, H.pylori must avoid both the innate
and adaptive immune responses.
H. pylori lipopolysacharide act as molecular
mimics of human glycan.
Nilsson et al. (2008), sweden

10. Clinical outcome of H.pylori

Acute H. Pylori infection- The infection is usually
acquired in early childhood. Infection is usually
accompanied by diarrohea, slowing of weight gain.

Chronic gastritis- After the acute phase, majority of
patients are not able to clear H.Pylori from the
stomach and this leads to persistent infection and
chronic gastritis.

11. Characteristics of H.pylori mediated human disease
Bauer et al. (2011) Hindawi publishing corporation, Germany