HELICOBACTER PYLORI: CHARACTERISTICS, MORPHOLOGY, HABITAT - BIOLOGY - 2025

Helicobacter pylori is a Gram negative helical bacterium, involved in the development of gastritis, peptic ulcers and associated with gastric cancer. It was discovered in 1983 by Australian pathologists Robin Warren and Barry Marshall when examining gastric mucosa from human stomachs.

Even Marshall experimented with himself, ingesting material contaminated with the bacteria, where he found that it caused gastritis, and was able to verify the presence of the bacteria in his own stomach biopsy. He also found that it responded to antibiotic treatment.

Helicobacter pylori

With this they dismantled old theories that claimed that gastritis was caused by consuming spicy foods or by stress. For this reason, in 2005 Warren and Marshal were awarded the Nobel Prize in Medicine.

General characteristics

Due to its great similarity to the genus Campylobacter, it was initially called Campylobacter pyloridis and later Campylobacter pylori, but was later reclassified to a new genus.

Helicobacter pylori infection is widely distributed in many mainly underdeveloped countries and is one of the most frequent infections in man, which usually occurs from childhood.

It is thought that once the microorganism is acquired for the first time, it can remain for years or for a lifetime, in some cases asymptomatic.

On the other hand, the stomach does not seem to be the only place where the microorganism can be harbored, it is believed that H. pylori can consolidate in the mouth before colonizing the stomach.

Likewise, it is possible that H. pylori present in the oral cavity could re-infect the stomach after treatment. This is reinforced by finding that some asymptomatic children have isolated the microorganism from dental plaque.

However, although Helicobacter pylori infection is asymptomatic in some people, it is not harmless, since it has been associated with 95% of duodenal ulcers, 70% of peptic ulcers and 100% of chronic gastritis of antral location.

Furthermore, Helicobacter pylori has been classified as a class I carcinogen by the International Agency for Research on Cancer, due to its association between infection and gastric cancer.

Habitat

Phylum: Proteobacteria

Class: Epsilonproteobacteria

Order: Campylobacterales

Family: Helicobacteraceae

Genus: Helicobacter

Species: pylori

Morphology

Microorganisms can be observed in tissue sections, and the mucosa will present pathognomonic characteristics of their presence.

The drawback is that the distribution of H. pylori in the stomach is not uniform.

Rapid urease test

It is a method of indirect detection of the bacteria.

Portions of the samples can be immersed in urea broth with a pH indicator (Phenol Red) and the results can be observed in less than an hour.

The urea broth medium turns from yellow to fuchsia due to the change in pH caused by the production of ammonia from urea, by the action of urease.

The sensitivity of this test depends on the bacterial load in the stomach.

Culture of gastric mucosa samples

Part of the sample taken by endoscopy can be destined to be cultured. A negative culture is the most sensitive indicator of a post-therapy cure.

The gastric or duodenal biopsy sample must be recent and its transport should not take more than 3 hours. They can be stored for up to 5 hours at 4ºC and the tissue must be kept moist (container with 2 mL of sterile physiological saline).

Before sowing the sample, a mash must be done to obtain greater sensitivity. The sample can be seeded on Brucella agar, brain heart infusion, or soy trypticase supplemented with 5% sheep or horse blood.

Polymerase chain reaction (PCR).

Tissue sections can be subjected to molecular biology techniques for the detection of DNA of the microorganism.

The advantage of PCR is that it can be used in the analysis of samples such as saliva, allowing the diagnosis of H. pylori in a non-invasive way, although the fact that the bacteria is found in saliva is not necessarily an indication of a stomach infection.

-Non-invasive methods

Serology

This method has a sensitivity of 63-97%. It consists of measuring IgA, IgM and IGG antibodies through the ELISA technique. It is a good diagnostic option, but it has limited utility for monitoring treatment.

This is because antibodies can remain elevated for up to 6 months after the organism has been killed. It has the advantage of being a quick, simple and cheaper method than those that require a biopsy endoscopy.

It should be noted that the antibodies generated against H. pylori are used for diagnosis but do not prevent colonization. Therefore, people who acquire H. pylori tend to suffer from chronic diseases.

Breath test

For this test the patient must ingest urea labeled with carbon (¹³ C or ¹⁴ C). When this compound comes into contact with the urease produced by the bacteria, it is transformed into marked carbon dioxide (CO ₂ C ¹⁴) and Ammonium (NH ₂).

Carbon dioxide passes into the bloodstream and from there to the lungs where it is exhaled through the breath. The patient's breath sample is collected in a balloon. A positive test is confirmatory of infection by this bacterium.

Modified breath test

It is the same as the previous one but in this case a colloid of 99mTc is added that is not absorbed in the digestive system.

This colloid allows the production of urea to be visualized exactly at the site of the digestive system where it is generated by means of a gamma camera.

Lifecycle

Helicobacter pylori within the body behaves in two ways:

98% of the H. pylori population resides free in the mucus of the stomach. This serves as a reservoir for adherent bacteria that will serve for transmission.

While 2% are attached to epithelial cells, which maintain the infection.

Therefore, there are two populations, adherent and non-adherent, with different survival characteristics.

Pathogeny

Once the bacteria enter the body, it can mainly colonize the gastric antrum, using the virulence factors that it has.

The bacteria can last a long time installed in the gastric mucosa, sometimes for life without causing discomfort. It invades and colonizes the deep layers of the gastric and duodenal lining mucus through proteases and phospholipases.

It then attaches itself to the superficial epithelial cells of the stomach lining and duodenum, without invading the wall. This is a strategic location that bacteria adopt to protect themselves from the extremely acidic pH of the stomach lumen.

Concomitantly at this site the bacteria unfold the urea to further alkalize its environment and remain viable.

Most of the time, a continuous inflammatory reaction occurs in the gastric mucosa, which in turn alters the mechanisms of regulation of gastric acid secretion. This is how certain ulcerogenic mechanisms are activated, such as:

The inhibition of parietal cell function through the inhibition of somatostatin, where the inadequate production of gastrin is favored.

The ammonia produced, plus the VacA cytotoxin mistreat epithelial cells, thus causing lesions in the gastric or duodenal mucosa.

Thus, degenerative changes of the epithelial surface are observed including mucin depletion, cytoplasmic vacuolization, and disorganization of the mucus glands.

Inflammatory infiltrate

The aforementioned injuries result in the mucosa and its lamina propria being invaded by a dense infiltrate of inflammatory cells. Initially the infiltrate may be minimal with only mononuclear cells.

But later the inflammation can spread with the presence of neutrophils and lymphocytes, which cause damage to the mucous and parietal cells and there may even be formation of microabscesses.

The CagA cytotoxin for its part enters the gastric epithelial cell, where multiple enzymatic reactions are triggered that cause the reorganization of the actin cytoskeleton.

The specific mechanisms of carcinogenesis are unknown. However, long-term inflammation and aggression are believed to lead to metaplasia and eventually cancer.

Pathology

In general, chronic superficial gastritis begins within a few weeks or months after the bacteria have settled. This gastritis can progress to a peptic ulcer and subsequently lead to gastric lymphoma or adenocarcinoma.

Likewise, Helicobacter pylori infection is a condition that predisposes to MALT lymphoma (Mucosal Associated Lymphoid Tissue Lymphoma).

On the other hand, the latest studies mention that Helicobacter pylori causes extragastric diseases. These include: iron deficiency anemia and idiopathic thrombocytopenia purpura.

Also skin diseases such as rosacea (the most common skin disease associated with H. pylori), chronic prurigo, chronic idiopathic urticaria, psoriasis among others. In pregnant women it can cause hyperemesis gravidarum.

Other less frequent sites in which it is believed that H. pylori may have some role in causing pathology is at the level of:

Middle ear, nasal polyps, liver (hepatocellular carcinoma), gallbladder, lungs (bronchiectasis and COPD chronic obstructive pulmonary disease).

It has also been linked to eye disease (open-angle glaucoma), cardiovascular diseases, autoimmune disorders, among others.

Clinical manifestations

This pathology can be asymptomatic in up to 50% of adults. Otherwise, in the primary infection it can cause nausea and upper abdominal pain that can last up to two weeks.

Later the symptoms disappear, to reappear some time later once the gastritis and / or peptic ulcer has been installed.

In this case the most common symptoms are nausea, anorexia, vomiting, epigastric pain and even less specific symptoms such as belching.

Peptic ulcer can cause severe bleeding that can be complicated by peritonitis due to leakage of gastric contents into the peritoneal cavity.

Contagion

People with Helicobacter pylori can shed the bacteria in their feces. In this way, drinking water could become contaminated. Therefore, the most important route of contamination of the individual is the fecal-oral route.

It is believed that it can be in water or in some vegetables that are usually eaten raw, such as lettuce and cabbage.

These foods may become contaminated by being watered with contaminated water. However, the microorganism has never been isolated from water.

Another uncommon route of contamination is oral-oral, but it was documented in Africa by the custom of some mothers to pre-chew their children's food.

Finally, contagion by the iatrogenic route is possible. This route consists of contamination by the use of contaminated or poorly sterilized material in invasive procedures that involve contact with the gastric mucosa.

Treatment

Helicobacter pylori in vitro is susceptible to a variety of antibiotics. Among them: penicillin, some cephalosporins, macrolides, tetracyclines, nitroimidazoles, nitrofurans, quinolones, and bismuth salts.

But they are inherently resistant to receptor blockers (cimetidine and ranitidine), polymyxin, and trimethoprim.

Among the most successful treatments, there are:

• Combination of medications, including 2 antibiotics and 1 proton pump inhibitor.
• The most commonly used combination of antibiotics is clarithromycin + metronidazole or clarithromycin + amoxicillin or clarithromycin + furazolidone or metronidazole + tetracycline.
• The proton pump inhibitor can be Omeprazole or Esomeprazole.
• Some therapies may also include the consumption of bismuth salts.

Therapy must be completed for at least 14 days, as recommended by the FDA. However, in some patients this therapy is difficult to tolerate. For them it is recommended to combine the treatment with the consumption of foods that contain probiotics.

These therapies are effective, however, in recent years resistance of Helicobacter pylori to metronidazole and clarithromycin has been recorded.

The microorganism can be eradicated, however reinfection is possible. In second therapies for reinfection, the use of levofloxacin is recommended.

References

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