Discovery history and taxonomy
The genus Helicobacter belongs to the family Helicobacteriaceae. The etymology of the name goes back to the Greek word helios, meaning "sun". These microorganisms were first discovered in the gastric mucosa by G. Bizzozero back in 1893. However, isolating them into an independent genus was achieved much later—in 1983 by researchers R. Warren and B.J. Marshall.
Initially, the bacteria were given the acronym CLO (Campylobacter-like organisms), as they closely resembled campylobacters in appearance. The genus received its final name only in 1989. The scientific community highly appreciated this work: in 2005, Warren and Marshall were awarded the Nobel Prize for discovering the role of this microbe in physiology and medicine. To date, more than 20 species of helicobacters have been described, but the species of greatest clinical significance for human pathology is H. pylori.
Morphological and tintorial properties
Helicobacters are small microorganisms measuring 2–5 × 0.5–1 µm that do not form spores. Their most important feature is pronounced polymorphism, i.e., the ability to change shape depending on environmental conditions:
- In living organism tissues (in vivo), they adopt a curved, S-shaped, or spiral form.
- When grown on artificial nutrient media (in vitro), they appear as rods.
- Upon the onset of unfavorable conditions, the bacteria transform into a coccoid form, which helps them survive.
The microbe is actively motile. For movement, it uses lophotrichous flagellation—a tuft consisting of 2–6 flagella located at one of the poles of the cell.
Physiology, cultivation, and biochemistry
By respiration type, Helicobacter is a microaerophile (requiring a reduced oxygen content at the level of 3–15%) and a capnophile (requiring an increased carbon dioxide content of 10–15%). The optimum temperature for its growth is $37^{\circ}C$.
The microorganism is extremely demanding regarding nutrient media. It is unable to utilize high-molecular-weight compounds, so complex media must necessarily contain additives: whole blood or serum, activated charcoal, soluble starch, and low-molecular-weight protein hydrolysate. In addition, the bacterium is strictly dependent on the presence of certain amino acids: arginine, leucine, valine, serine, and phenylalanine.
Biochemical activity has its own characteristics. Saccharolytic activity is completely absent—the microbe does not ferment sugars, and tricarboxylic acids serve as its source of energy. At the same time, the bacterium produces a number of enzymes: catalase, oxidase, alcohol dehydrogenase, and lipases.
Urease and other pathogenicity factors
The complex of pathogenicity factors ensures the bacterium's survival in the acidic environment of the stomach, colonization of the mucosa, and tissue damage. The key enzyme, most important species marker, and infection marker is urease. It is a multicomponent metal-containing enzyme possessing the highest activity among all bacterial ureases (accounting for up to 15% of the total cellular protein).
The role of urease in pathogenesis:
- Defense: creates a "cloud" of ammonia around the bacterium, neutralizing hydrochloric acid and raising the pH.
- Regulation: if the environment becomes excessively alkaline, the microbe turns on oxidases to re-acidify it.
- Damage: ammonium ions cause lysis of epithelial cells and destroy intercellular contacts.
- Inflammation: the enzyme acts as a chemoattractant, recruiting leukocytes and provoking their pro-inflammatory activation.
In addition to urease, aggression is provided by phospholipase A (destroys cell membranes), adhesins (responsible for attachment to the epithelium), and endotoxin (cell wall lipopolysaccharide).
Specific toxins and genetics
Helicobacter is characterized by high genetic diversity. Continuous selection of strains most tropic to a specific tissue occurs within the host organism, and adaptation is ensured by mutations.
Of particular importance are two specific toxins, which are also associated with bacterial resistance to the antibiotic clarithromycin:
- Vacuolating cytotoxin (VacA). This is a polypeptide that forms channels (pores) in the cytoplasmic membrane of the host cell. It disrupts membrane integrity, causes vacuole formation in the cytoplasm, and ultimately triggers apoptosis.
- Cytotoxin-associated gene A (CagA). This factor is associated with "pathogenicity islands". Its main function is the stimulation of pro-inflammatory cytokine production (such as IL-1$\beta$ and IL-8), which maintains the chronic inflammatory process.
Briefly: answers to topical questions
What aggression and defense enzymes does Helicobacter pylori produce?
Helicobacter pylori produces enzymes involved in surviving the acidic environment of the stomach and causing tissue damage.
- Urease — neutralizes hydrochloric acid with ammonia, causes lysis of epithelial cells, and provokes inflammation.
- Oxidase — participates in acidifying the environment when it becomes excessively alkaline.
- Phospholipase A — destroys membranes.
- Catalase and alcohol dehydrogenase — are produced by H. pylori.
Which pathogenicity factors ensure the adhesion of Helicobacter to the gastric epithelium?
Adhesion of Helicobacter pylori to the gastric epithelium is provided by adhesins, which ensure the attachment of the bacterium to the epithelium.
Which gastrointestinal diseases are associated with Helicobacter pylori infection?
Associated with Helicobacter pylori infection are:
- Chronic Helicobacter-associated gastritis, including type B bacterial gastritis.
- Atrophic gastritis.
- Peptic ulcer disease of the stomach and duodenum.
- Gastric cancer, including invasive intestinal-type adenocarcinoma developing through the Correa cascade.
- Gastric MALT lymphoma.
Which laboratory diagnostic methods are used to detect Helicobacter pylori?
To detect Helicobacter pylori, the following are used:
- Histological examination of a gastric mucosa biopsy specimen.
- Rapid urease test (CLO test).
- 13C-urea breath test.
- Determination of H. pylori antigen in stool.
Which antibacterial drugs are included in standard Helicobacter pylori eradication regimens?
First-line Helicobacter pylori eradication regimens include:
- Clarithromycin — used in standard triple and concomitant therapy.
- Amoxicillin — included in standard triple, enhanced triple, and concomitant therapy.
- Metronidazole — included in quadruple therapy and concomitant therapy.
- Tetracycline — included in classical bismuth-containing quadruple therapy.
These drugs are combined with a proton pump inhibitor; a bismuth preparation is also used in some regimens.
To remember H. pylori's respiratory requirements, use the mnemonic: «Low Oxygen — Microaerophile, High CO2 — Capnophile».
Class and exam questions
Why doesn't Helicobacter die in the acidic environment of the stomach?
The bacterium produces the enzyme urease, which breaks down urea, releasing ammonia. Ammonia neutralizes hydrochloric acid and creates a protective alkaline cloud around the microbe.
What shape does the pathogen have?
Helicobacter exhibits polymorphism. In the human body, it is spiral- or S-shaped, on nutrient media it becomes rod-shaped, and under stress, it transforms into a coccus.
Does Helicobacter ferment sugars?
No, its saccharolytic activity is completely absent. The energy source for the bacterium consists exclusively of tricarboxylic acids.
What else to study on this topic
- Mechanisms of genetic variability and selection of tropic strains
- The role of oxidases in the regulation of acidity around the bacterial cell
- Features of H. pylori cultivation and the composition of complex nutrient media
- The relationship of VacA and CagA toxins with clarithromycin resistance
- Pathogenesis of the destruction of intercellular contacts in the gastric epithelium
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