H.pylori - Transmission, Persistence, Clinical outcome

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H. Pylori Transmission Persistence Clinical outcome By, Bharati Singh

Transcript of H.pylori - Transmission, Persistence, Clinical outcome

Page 1: H.pylori - Transmission, Persistence, Clinical outcome

H. Pylori

TransmissionPersistenceClinical outcome

By, Bharati Singh

Page 2: H.pylori - Transmission, Persistence, Clinical outcome

Source of infection of H. pylori

Crowded living conditionPoor living conditionLarge family sizeLack of hot running water

Route of transmission

Most H. pylori transmission occur in childhood Gastric- oralOral-oralFecal-oral

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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

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Prevalence of H. pylori infection by age in developed and developing countries

Logan et al. (2001) BMJ clinical review, 323

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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.

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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.

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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.

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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 .

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Stomach mucosa colonized by Helicobacter Pylori

Montecucco et al. (2001) Nat Rev Mol Cell Biol 2, 457-466 

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PersistanceTo 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

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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.

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Characteristics of H.pylori mediated human disease

Bauer et al. (2011) Hindawi publishing corporation, Germany