Helicobacter Pylori Infection; Short Note for Undergraduate Medical Student

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Helicobacter pylori Infection

By: Hariz Hizami Hatta

1.      Characteristics:

a)    gram negative

b)     microaerophilic (require environment with lower level of oxygen)

c)      bacilli (cork-crew shape)

d)     has flagella (motility)

e)     ROT: faecal-oral

 

2.     Disease associated with H. pylori:

a)     chronic gastritis

b)     peptic ulcer disease

 

·         It has lipopolysaccharide (LPS) on cell surface that are less mitogenic, pyrogenic and toxic compare to other Enterobacteriaceae

·         Has ability to neutralize gastric acid by secreting urease that will be converted into ammonia (alkaline), subsequently can withstand the acidity and continue causing inflammation to the epithelial cells

 

3.     Investigations of H. pylori infection:

Non-invasive test;

To detect bleeding

a)     CBC

b)     Rectal exam

c)      Faecal Occult Blood Test (FOBT) – To check blood in stool that cannot be seen with naked eyes. Faces smeared on treated paper, which reacts to hydrogen peroxide. If blood is present, the paper turns blue.

To detect the presence of H. pylori

a)     Urea breath test

-         2 weeks before test, pt must discontinue taking any antibiotics, PPIs

-         procedure: pt swallow substance containing urea treated with carbon atoms. If there’s H. pylori infection, the urea will be converted into carbon dioxide that will be detected and recorded in pt’ s exhaled breath after 10 minutes

-         pt need to fast overnight and baseline breath sample is obtained first. result will be based on increase of carbon dioxide in the breath

 

b)     Stool test

-         detect genetic fingerprints of H. pylori

-         can be as accurate as the breath test

Indications:

·         patient with dyspepsia + history of active ulcers + other RFs

·         smokers with persistent pain on an empty stomach

·         regular NSAIDs users with dyspepsia

·         risk for stomach cancer + dyspepsia

·         patient with dyspepsia longer than 4 weeks

Invasive test:

a)     Endoscopy (oesophagogastroduodenoscopy, OGD)

 

Thins tube tipped with a tiny video camera to evaluate the oesophagus, stomach and duodenum. Most commonly combined with biopsy to look for peptic ulcers, bleeding, cancer or to confirm presence of H. pylori.

 

Indicated for pt with dyspepsia as well as RF for ulcers, stomach cancer or both. Pt with unexplained weight loss, dysphagia and anaemia

 

b)    Rapid urease test

-         Campylobacter-like organism (CLO test)

-         rapid detection of ammonia after converted from urea by H. pylori using urease

-         reagent that contain urea and phenol red (weak acid) will react with tissue biopsy specimen that contain H. pylori. H. pylori convert urea into ammonia that is alkaline with urease enzyme and will neutralize the phenol red (weak acid)

-         colour change from yellow to pinkish or purplish

 

§  can be false negative with recent use of PPIs, antibiotics or bismuth compounds

 

c)    Blood tests

 

To measure antibodies to H. pylori. Use ELISA

Diagnostic accuracy 80 to 90%

 

d)   Histological identification

 

Can use Warthin-Starry, H&E and Giemsa stains. To exclude malignancy

 

e)     H. pylori culture

 

f)       Molecular methods

 

g)     PCR

 

4.    Virulence factors

 

a)     Urease enzyme

-         convert urea into bicarbonate and ammonia (alkaline) that can neutralize gastric acid

-         can be detected in breath test

 

b)     Inability of body’s natural defence

-         WBC, Killer T cells etc. cannot reach the bacterium in the mucus lining of stomach

 

c)      Adhesins (LPS)

-         adhere (bind) to specific receptors on epithelial cells

 

d)     Flagella for motility

 

e)     Exotoxin (Vacuolating toxin VacA) – gastric mucosal injury

 

f)       Effectors (CagA) – actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition

 

g)     Nutrient supply

 

Virulence Factors

Descriptions

Flagella

Motility, allow rapid movement in viscous solutions such as the mucus layer

Urease

Metabolize urea to produce ammonia and carbon dioxide. Withstand the acidity of stomach via neutralization

Adhesins

Adheres to receptors in the gastric epithelium by means of adhesins

Vacuolating Cytotoxin (VacA)

·         Able to induce vacuole formation in eukaryotic cells, membrane channel formation leading to release of cytochrome c release from mitochondria eventually apoptosis of cells.

·         Pro-inflammatory response and inhibit T cell activation

Cytotoxin-associated gene A (CagA)

·         Alters intracellular signal transduction pathways that facilitate the malignant transformation of gastric epithelial cells

·         Increase IL-8 secretion which predisposes to genetic instability and carcinogenesis

 

5.      Treatment

 

·         Triple therapy (PPIs + 2 antibiotics)

-         antibiotics: amoxicillin, clarithromycin, metronidazole, tetracycline

-         PPIs: reduce gastric acid secretion in the stomach

 

·         Histamine (H2) receptors blockers; reduce acid secretion

 

·         Bismuth subsalicylate: anti diarrheal (common OTC medication)

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