Helicobacter pylori
(Helicobacter pylori bacteria. Coloured scanning electron micrograph of H pylori bacteria)

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family : Helicobacteraceae
Genus: Helicobacter
Species: H. pylori

- Gram-negative
- micro-aerophilic (H. pylori needs oxygen to survive but lives in environment containing less oxygen level than is present in the atmosphere)

Chromosome (base pair)
Open Reading Frame
GC Content

1 667 867
1 590

1 549 666
1 548

1 652 983
1 515

1 673 997
1 711

In 1873, a famous anatomist called Bizzozero, first described spirochetes in dogs gastric mucosa.

In 1940, Feedberg, Baron, and Doenges found these organisms in gastric mucosa of macaques and other species. They were disputed because some doctors and scientists commented on cases of remission of ulcer disease after patients have received treatment against syphilis. (Syphilis treatments consisted of heavy metal such as mercury and arsenic). It was believed that ulcer disease was caused by an excess of acid in the stomach.
But, in the 1980s, Barry Marshall and Robin Warren discovered that the Peptic Ulcer Disease (PUD) was caused by Helicobacter pylori and in 2005, they received the Nobel prize in Physiology or Medicine for their research.
H. pylori is the causative agent of gastritis. This bacteria is able to survive in human stomach in a very low pH (between 1.5 and 4.5)

Transmission of H. pylori
It is believed that H. pylori is strictly human pathogens with few reservoirs such as pigs and non-human primates. Two modes of transmission have been proposed:
- fecal-oral transmission (H. pylori can survive in the intestinal tract)
- oral-oral transmission

This pathogen use urease for stomach colonization. This enzyme allow bacteria to survive under very low acidic conditions

Half of the world population is infected by this bacteria which makes it the most common infectious micro-organism. More than 50% of H. pylori strains contain the "cag pathogenecity island and give to patient a stronger immune response in their stomach and thus greater chance to developp gastric ulcer.
Symptoms: dyspepsia which refers to an indigestion and a chronic pain upper the abdomen.
Diagnostics using:
- Antibody test (such as urine ELISA test)
- Non-invasive urea breath test. The urea breath test is based on the ability of H. pylori to convert urea to ammonium. Urea is labelled with a carbon 14 or 13 isotope. Patients swallow it and detection of labelled carbon dioxide in exhaled breath show that urea was converted to ammonium by an enzyme called urease.

H. pylori can induce cancer by two ways. Some studies show that free radicals near this bacteria induce DNA mutations and these mutations promote cancer of the host cell. Also, this pathogen can alter cell adhesion of the gastric epithelium and thus induce cell migration.

To cure peptic ulcer cause by H. pylori, patients are treated with three different drugs:
1) proton pump inhibitors (omeprazole),
2) a marcolide antibiotics (clarithromycin) which interfers with bacteria protein synthesis,
3) a beta-lactam antibiotic (amoxicillin).

It was recently demonstrated that the ingestion of lactic acid bacteria prevent negative effects of H. pylori. These lactic acid bactera are found in fermentated food such as lactic products.

In 2000, using murine models, researchers found that lipoprotein 20 can be a candidate vaccine and enhance immune response against H.pylori.
In 2001, a vaccine using a recombinant urease was produced in order to prevent infection. However, this vaccine activated mice immune system but in human the vaccine has not had the desired result.
Image_54_M&M.png(Prinz et al., 2003)
alum=aluminum hydroxide ; LT= E. coli heat-labile enterotoxin


(1) "Helicobacter pylori: physiology and genetics" By Harry L. T. Mobley, George L. Mendz, Stuart L. Hazell, 2001
(2) Helicobacter pylori 26695, complete genome". National Center for Biotechnology Information.
(3) Helicobacter pylori J99, complete genome". National Center for Biotechnology Information.

(4) Genome of Helicobacter pylori strain 908, Journal of Bacteriology
(5) Tomb JF, White O, Kerlavage AR, Clayton RA, Sutton GG, (1997), The complete genome sequence of the gastric pathogen Helicobacter pylori, Nature, 539-47
(6) Pradip K. Bardhan, (1997), Epidemiological Features of Helicobacter pylori Infection in Developing Countries, Clinical Infectious Diseases, 25, 973–8
(7) C. Prinz, N. Hafsi, P. Voland, (2003), Helicobacter pylori virulence factor and the host immune response: implications for therapeutic vaccination, 11, No.3, 134-138