SN4
SHORT NOTE
5M
★ High-yield
Describe Helicobacter pylori with its pathogenesis, associated diseases and diagnosis.
The Organism
- A gram-negative, curved or S-shaped (spiral) bacillus with multiple sheathed polar flagella giving rapid corkscrew motility through mucus
- Microaerophilic; slow-growing and fastidious
- Strongly urease positive — the central property, and the basis of both its survival and almost every test used to detect it
- Also oxidase and catalase positive
- Colonises the gastric antrum, living in the mucus layer adjacent to the epithelium rather than invading it
- Prevalence exceeds 70% in India, acquired in childhood by the faecal-oral or oral-oral route, and associated with crowding and poor sanitation
- Urease splits urea into ammonia and carbon dioxide → Ammonia neutralises gastric acid in the immediate surroundings → The organism survives the most hostile environment in the body and burrows through mucus using its flagella → It adheres to gastric epithelium
- CagA and VacA are injected or secreted, causing cell injury → Chronic active gastritis → Depending on the pattern — antral gastritis raises acid and causes duodenal ulcer
- body-predominant gastritis causes atrophy, reduces acid and predisposes to gastric ulcer and carcinoma
CLINICAL PEARL
The enzyme that lets it survive is the enzyme that betrays it. urease is what allows H. Pylori to neutralise acid and colonise the stomach — and it is also the basis of the rapid urease test, the urea breath test and the histological stains. A single adaptation is simultaneously the organism's survival mechanism and the most convenient diagnostic handle available.
Associated Diseases
- Chronic gastritis — in essentially all colonised individuals, though most remain asymptomatic
- Peptic ulcer — associated with over 90% of duodenal ulcers and about 70% of gastric ulcers; eradication cures the ulcer disease and prevents recurrence, which transformed a chronic relapsing surgical condition into a curable infection
- Gastric adenocarcinoma — classified by the WHO as a group 1 carcinogen; the sequence runs chronic gastritis, atrophy, intestinal metaplasia, dysplasia, carcinoma
- Gastric malt lymphoma — remarkably, low-grade disease frequently regresses with eradication alone, without chemotherapy; a unique example of an antibiotic curing a malignancy
- Other associations — unexplained iron deficiency anaemia and immune thrombocytopenia, in which eradication is recommended
Diagnosis
| Test | Type | Comment |
|---|---|---|
| Rapid urease test (CLO test) | Invasive — on biopsy | Biopsy placed in urea with an indicator; a colour change within minutes to hours. Rapid and cheap |
| Histology | Invasive | Giemsa, Warthin-Starry or immunostain; also shows gastritis, atrophy, metaplasia and malignancy |
| Culture | Invasive | Difficult and slow, but the only way to obtain antibiotic sensitivities |
| Urea breath test | Non-invasive — the test of choice | Labelled urea is swallowed; urease releases labelled CO2 in the breath. Detects active infection and is the preferred test of eradication |
| Stool antigen | Non-invasive | Detects active infection; useful in children and for confirming cure |
| Serology (IgG) | Non-invasive | Cannot distinguish current from past infection and remains positive after successful treatment, so it must not be used to confirm eradication |
- Proton pump inhibitors, antibiotics and bismuth cause false negatives and must be stopped — antibiotics and bismuth for 4 weeks, and proton pump inhibitors for 2 weeks — before breath, stool, urease or histological testing
Treatment and Applied Aspects
- Standard triple therapy — a proton pump inhibitor with clarithromycin and amoxicillin (or metronidazole) for 14 days
- Quadruple therapy — proton pump inhibitor, bismuth, tetracycline and metronidazole, used where clarithromycin resistance is high, which now includes much of India
- Acid suppression is part of the treatment, not merely symptomatic: the antibiotics work far better at a higher gastric pH
- Confirm eradication at least 4 weeks after treatment by urea breath test or stool antigen — never by serology
- Resistance is rising rapidly in India, particularly to clarithromycin and metronidazole, largely from their widespread use for other indications; this is shifting practice towards quadruple and sequential regimens
- Do not test and treat indiscriminately; test those with peptic ulcer, malt lymphoma, a family history of gastric cancer, unexplained iron deficiency, or requiring long-term NSAIDs — eradicating in every dyspeptic patient drives resistance without proportionate benefit
All questions in Gram-negative Bacteria
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- SN2Describe Klebsiella and Proteus with their characteristics and clinical importance. ★
- SN3Describe Pseudomonas aeruginosa with its virulence factors, infections and treatment. ★
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- SN5Describe ESBL and carbapenemase-producing organisms with their detection and treatment. ★
- SN6Describe Campylobacter and Yersinia with their clinical features and complications. ★
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