Helicobacter pylori: Morphology and Identification, Pathogenesis and Pathology, Clinical Findings, Diagnostic Laboratory Tests, Treatment, Epidemiology and Control. Flashcards
(7 cards)
Helicobacter pylori: morphology and identification
Helicobacter pylori is a Gram-negative, curved or spiral-shaped rod with multiple sheathed polar flagella, giving it strong motility. It is microaerophilic and catalase-, oxidase-, and urease-positive. On microscopy, it appears curved or ‘comma-shaped.’ It grows on enriched media like Skirrow’s or chocolate agar under microaerophilic conditions (5% O₂, 10% CO₂, 85% N₂). Its urease activity is a key feature for identification.
Helicobacter pylori: pathogenesis and pathology
H. pylori colonizes the gastric mucosa and survives acidic conditions by producing large amounts of urease, which breaks down urea to produce ammonia, neutralizing stomach acid locally. It adheres to gastric epithelial cells using adhesins and damages them with cytotoxins like CagA (cytotoxin-associated gene A) and VacA (vacuolating cytotoxin A). The resulting inflammation contributes to chronic gastritis, peptic ulcers, and gastric carcinoma. CagA-positive strains are more virulent and associated with adenocarcinoma.
Helicobacter pylori: clinical findings
H. pylori infection can be asymptomatic but is commonly associated with chronic gastritis and peptic ulcer disease (especially duodenal ulcers). It is also linked to gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. Symptoms include epigastric pain, bloating, nausea, vomiting, and, in ulcer cases, hematemesis or melena.
Helicobacter pylori: diagnostic laboratory tests
Diagnosis can be invasive or non-invasive. Invasive tests include biopsy during endoscopy with rapid urease test (CLO test), histology, and culture. Non-invasive tests include the urea breath test (using ¹³C- or ¹⁴C-labeled urea), stool antigen tests, and serologic antibody tests (less useful for current infection). The urea breath test and stool antigen tests are preferred for both diagnosis and post-treatment follow-up.
Helicobacter pylori: treatment
Standard treatment is ‘triple therapy’ with a proton pump inhibitor (PPI) plus two antibiotics (usually clarithromycin and amoxicillin or metronidazole) for 10–14 days. If resistance or failure occurs, ‘quadruple therapy’ (PPI, bismuth, tetracycline, and metronidazole) is used. Treatment eradicates infection and promotes ulcer healing, and may reduce cancer risk.
Helicobacter pylori: epidemiology
H. pylori infects over half the global population, with higher prevalence in developing countries. Transmission is primarily oral-oral or fecal-oral, often acquired in childhood. Infection persists without treatment. Risk factors include low socioeconomic status, poor sanitation, and crowded living conditions.
Helicobacter pylori: control
There is no vaccine. Control relies on identification and eradication of infection in symptomatic individuals, particularly those with ulcers or malignancy risk. Good hygiene, safe food and water, and improved sanitation help prevent transmission. Family members of infected individuals may also be screened.