HELICOBACTER PYLORI

- Found in the stomach of over half the world’s population → can cause inflammation of
the stomach lining → peptic ulcer
- Causative agent of most common chronic infection in humans; common cause of
duodenal, gastric ulcers, chronic gastritis

Characteristic
- Gram (-) curved rod shape
- 2-7 unipolar sheathed flagella (H-antigen): provide motility, chemotaxis (sense
pH, move bacteria towards beneficial environment)
- Positive for urease, catalase and oxidase, non invasive
- Microaerophilic → requires oxygen, low concentrations than present in atmosphere
- Lipopolysaccharide (LPS): promotes adherence, causes inflammation
- Coccoid form: more resistant form; occurs as adaptation to hostile environment outside
human body
- Urease: important for survival, colonization
- Mucolytic enzymes: allow passage through mucus layer to gastric epithelium
- Adhesive protein (Hop proteins)
- Vacuolating cytotoxin A (VacA): damages epithelial cells; disrupts tight junctions, causes
apoptosis
- Cytotoxin associated gene CagA: triggers inflammation
- Type IV secretion system: pili-like structure for injection of effectors (e.g. CagA)
- Protease, lipases
- Biofilm formation

Transmission
- Fecal-oral, gastro-oral, oral-oral transmission
- Contamination of food and water or directly (fecal matter, vomitus, saliva)
- Also found in municipal water in endemic areas of infection with PCR technique

Pathogenesis
- H.pylori once in stomach → migrate to regions where pH is less acidic (like the antrum
→ fewer parietal cells) → use adhesin protein to stick to the surface of foveolar cells
where it can release a number of virulence factors (for survival and can damage
mucosa)
- Bacterial urease hydrolyzes gastric luminal urea to form ammonia and CO2 → ↑ gastric
pH (base) → formation of protective layer around bacteria → survival in hostile gastric
environment
- ↑ pH → mucin liquefies → H.pylori passes through mucous layer to surface epithelium
via bacterial flagella, mucolytic enzymes → attaches to specific gastric epithelial cell
receptors via surface adhesins (Hop proteins) → release of proteases (VacA → cause
epithelial death, CagA) → induce inflammatory immune response → tissue injury →
gastritis
 - Chronic inflammation, ↑ TNF, ↑ IL-6, ↑ bacterial proteases → excessive tissue damage,
cell mutation → intestinal metaplasia → carcinoma
- Gastric mucosa-associated lymphomas → due to persistent immune stimulation of
gastric lymphoid tissue
- MALT lymphoma, adenocarcinoma
- Ulcers: inflammation stimulates G cells to secrete gastrin → parietal cells produce
hydrochloric acid
- Corpus gastritis → gastric ulcer
- Antral gastritis → duodenal ulcer
- Rare: long standing ulcers in pyloric canal → sometimes have so much
edema or scarring that they obstruct the normal passage of gastric
contents into the duodenum
- Deep ulcers → erode underlying blood vessels → perforation

Signs and Symptoms

- Majority of cases → asymptomatic (may play a role in the natural stomach ecology)
- Acute infection: upper abdominal pain, nausea, loss of appetite
- Chronic infection (CagA, VagA):
- Chronic gastritis: upper abdominal pain, nausea, bloating, vomiting/melena (black
stool)
- Peptic ulcers: stomach pain/ache; occurs with empty stomach, between meals,
early mornings
- If blood vessel erodes: blood in vomit or feces
- If nearby artery erodes: rapid blood loss and shock
- Perforation: air collects under diaphragm → irritate phrenic nerve → referred pain
in shoulder
- Can lead to iron deficiency anemia: bacteria sequester dietary iron

Diagnosis
- Blood antibody test
- Stool antigen test
- Carbon urea breath test → ingest 14C or 13C labelled urea, which bacterium
metabolizes, yielding labelled CO2 detectable in breath
- Urine ELISA test
- Upper GI endoscopy
- Culture:
- Isolation specimen: vomitus, diarrheal stools. Gastric biopsy
- Media: blood agar/selective Skirrow’s media incubated at 37℃ in 5% oxygen;
small, uniformly sized, translucent bacterial colonies

Treatment
- No clinical symptoms → not treated
- Family history of GI cancer or clinical symptoms → TRIPLE THERAPY: antacid/acid
reducing drugs (H2-receptor antagonists/proton pump inhibitor) + 2 antibiotics
- Amoxicillin + Clarithromycin + Omeprazole/pantoprazole (if penicillin sensitive →
replace amox with metronidazole)
- Bismuth salicylate + Metronidazole + Tetracycline
- Ranitidine bismuth citrate + Tetracycline + Clarithromycin/Metronidazole