Helicobacter Pylori (Student Notes)

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Helicobacter pylori are spiral/curve-shaped, gram-negative rods. They are motile, and their mobility is provided by multiple polar flagella (lophotrichous flagella).

Helicobacter pylori is the only bacteria known to be able to colonize the human stomach. Here it greatly increases the chance of developing gastric and duodenal ulcers, as well as gastric carcinoma. Luckily, it can be eradicated using a combination of antibiotics.

Laboratory features

The bacterium is microaerophilic, which means they thrive in environments with lower O2 (5%) and increased CO2 (10%). In addition, the bacterium has an optimal pH range between 6-7.

It can be grown on various nutrient agars as well as on a selective skidrow medium, which is a medium containing various antimicrobial substances inhibiting the growth of other bacterias.

Helicobacter pylori are fairly slow-growing. They generally require an incubation period ranging from 3-6 days, after which they form round, convex, watery, grey/colorless colonies.

The bacterium is both oxidase and catalase-positive. This is of diagnostic value as it enables differentiation with biochemical tests (oxidase & catalase test).

More importantly, Helicobacter pylori express strong urease activity which is important for its ability to survive in the stomach and has great clinical diagnostic value (more later).

This urease activity allows the bacterium to survive in the acidic environment of the stomach. This is because the cleavage of urea generates CO2 and ammonia (NH3) which makes the microenvironment more basic (increases the pH) to the point where the bacteria can survive.

Virulence factors

Helicobacter pylori possess various virulence factors, some of which are not entirely understood yet. What we do know is that some strains (about 50%) become more virulent due the acquisition of a Cag pathogenicity island. 

Pathogenicity islands are sequences of DNA that are passed between bacterias by means of horizontal gene transfer. This is the exchange of genetic material between cellular organisms without there being any reproduction(which is vertical gene transfer).

The Cag pathogenicity island acquired by Helicobacter pylori contains a sequence of DNA coding for cytotoxin-associated gene A (CagA).

This is a protein that likely contributes to the pathogenicity of the bacteria, including activating protooncogenes which can contribute to the development of cancer.

Moving on, the bacterium also possesses 2 important adhesins, babA and sabA. These facilitate the attachment of the bacterium to the gastric/duodenal epithelium where they can form biofilms.

Their strong urease activity can also be considered a virulence factor as it enables the bacteria to colonize the stomach mucosa. Also, the release of ammonia irritates the gastric mucosa, contributing to the pathogenicity.

Finally Helicobacter pylori also releases various protease enzymes that can damage gastric epithelial cells. It also releases a cytotoxin called vacuolating cytotoxin A (VacA) which can damage epithelial cells.


Helicobacter pylori is common all around the world, however, most are asymptomatic carriers. The bacterium is believed to be transmitted from humans to humans as no other reservoir has been identified.

Once the bacterium enters the stomach, its motility enables it to invade the protective mucous layer of the stomach or duodenum where the pH is more favourable, and colonize the epithelial surface.

Once it colonizes the gastric mucosa, its urease activity, the release of protease enzymes and toxin production irritates the epithelial cells, which leads to inflammation of the mucosa.

Continuous production of irritants (proteases and toxins) leads to a chronic inflammation that can lead to the development of gastritis. This can progress to ulceration over time, either in the stomach or duodenum.

In addition to causing ulceration, Helicobacter pylori infection appears to be a risk factor for the development of gastric carcinoma and gastric B-cell lymphoma (MALT associated lymphomas).

Keep in mind that colonization with Helicobacter pylori does not necessarily lead to the development of gastric/duodenal ulcers as up to 80-85% are asymptomatic carriers. However, there is a strong correlation between the development of gastric/duodenal ulcers and Helicobacter pylori infections.

Nearly all patients with gastric ulcers and about 95% of patients with duodenal ulcers turn out to be infected with Helicobacter pylori.


In order to determine whether a patient has a Helicobacter pylori infection, various diagnostic tests can be performed to detect the presence of the bacteria.

First of all, biopsies can be taken during gastroscopy examination, after which the sample is stained with Giemsa stain or silver nitrate impregnation which visualises the bacteria on a direct smear.

In addition, the sample can be checked for urease activity. The sample is placed onto an urea containing medium together with a colour indicator. Change of colour represents urease activity which indicates presence of the bacteria. THis is the simplest and fastest test.

A less invasive test is detection of anti-Helicobacter pylori antibodies from the patient’s serum which can be done with indirect ELISA tests.

A positive result does not necessarily indicate infection, however, negative results exclude HP infection. In addition, it can be used to monitor whether efforts to eradicate the bacteria was successful.

Finally, a commonly used test is the urea breath. Here the patient ingest a solution containing radioactive labelled urea particles. If the bacteria is present, they will cleave the urea releasing radioactive labelled CO2. This Co2 is in turn exhaled by the patient and can be measured, resulting in a positive test.


If one of the diagnostic tests has confirmed the presence of Helicobacter pylori, it can be eradicated using a combination of antibiotics.

Elimination of the bacterium is not necessary in patients with no symptoms. However, patients with ulcers caused by Helicobacter pylori infections are usually put on a 14 treatment with proton pump inhibitors and a combination of the following antibiotics.

  • Clarithromycin + metronidazole
  • Amoxicillin + metronidazole
  • Doxycycline + metronidazole