Vibriões e curvos

Helicobacter pylori

Curved and spiral Gram-negative bacilli

Identification & Growth

Identification

Very rapid urease (urease test positive within minutes), catalase- and oxidase-positive

Growth Conditions

Selective media for gastric biopsy, microaerophilic atmosphere with high humidity, 3–7 days at 37 °C

Clinical Significance

Chronic gastritis, peptic ulcer, MALT lymphoma and gastric adenocarcinoma

Intrinsic Resistance

Trimethoprim, sulfonamides and vancomycin are inactive (they are used as selective agents in the medium)

Bench Alerts

EUCAST/BrCAST define MIC breakpoints (gradient test on Mueller-Hinton with blood), not disk diffusion
Clarithromycin resistance is the main determinant of failure — test before retreatment

Clinical Notes

Clinical presentations

Chronic active gastritis and the leading etiological factor for gastric and duodenal peptic ulcer disease.
Recognized risk factor for gastric adenocarcinoma and gastric MALT lymphoma.
Frequently associated with functional dyspepsia, although many carriers remain asymptomatic.

Specimens and collection

Endoscopic gastric biopsy (antrum and body) for rapid urease test, histology and culture, with proton pump inhibitor withheld for at least 2 weeks before testing where feasible.
Non-invasive tests: urea breath test (13C) and stool antigen test, useful for initial diagnosis and confirmation of eradication.
Culture with susceptibility testing is indicated after treatment failure or in areas of high clarithromycin resistance, requiring rapid transport in appropriate medium because the organism is a fastidious microaerophile.

Epidemiology and at-risk populations

One of the most prevalent chronic bacterial infections worldwide, transmitted predominantly oral-oral or fecal-oral, usually acquired in childhood.
Higher prevalence in low- and middle-income countries and associated with poor socioeconomic and sanitary conditions.
WHO classifies H. pylori as a group 1 carcinogen, reinforcing the rationale for screening and eradication in selected populations.

Resistance and therapeutic implications

Rising resistance to clarithromycin and metronidazole in many regions guides the choice of therapy regimen according to local resistance data.
Eradication regimens combine a proton pump inhibitor with two or more antimicrobials (triple therapy, bismuth-based quadruple therapy or concomitant therapy) per consensus guidelines.
EUCAST publishes breakpoints for H. pylori for selected agents; susceptibility testing by agar diffusion or E-test requires prolonged microaerophilic incubation.

Bench and reporting notes

Spiral, microaerophilic Gram-negative rod, urease-, catalase- and oxidase-positive, motile via multiple polar flagella.
The rapid urease test relies on the organism's intense urease activity and is the most widely used screening method during endoscopy.
Confirm eradication only at least 4 weeks after completing antimicrobials and 2 weeks off proton pump inhibitors, to avoid a false negative.

Sources

Educational decision-support content. It does not replace laboratory validation, current guidelines or review by the responsible professional.

FAQ: Frequently Asked Questions

How to identify Helicobacter pylori in the lab?

Helicobacter pylori is identified through very rapid urease (urease test positive within minutes), catalase- and oxidase-positive.

What are the intrinsic resistances of Helicobacter pylori?

This organism is naturally resistant to trimethoprim, sulfonamides and vancomycin are inactive (they are used as selective agents in the medium). These drugs should not be reported as susceptible.

Where is Helicobacter pylori commonly found?

It is typically associated with chronic gastritis, peptic ulcer, malt lymphoma and gastric adenocarcinoma.

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