H. pylori on the GI-MAP

The panel reports how much was detected, plus eight virulence-factor genes and resistance-associated markers. Here is what each part is, and what it deliberately does not decide.

Key facts

  • What it is: a bacterium that colonises the stomach lining.
  • On the GI-MAP: reported quantitatively by qPCR, on both the Standard panel and the targeted H. Pylori Profile.
  • Also reported: eight virulence-factor genes and resistance-associated markers.
  • What it does not do: decide whether you are treated, or with what. That is a prescribing decision.

Helicobacter pylori is a bacterium adapted to survive in the stomach, where most organisms cannot. It is common worldwide, frequently carried without symptoms, and is also associated with gastritis and peptic ulcer disease. That combination — common, often silent, sometimes consequential — is exactly why a detection result needs clinical context rather than a reflex.

What the GI-MAP reports

Three separate things, and it is worth keeping them apart:

What is reportedWhat it tells you
H. pylori quantity (qPCR)How much H. pylori DNA was detected in the sample, rather than a yes/no. Quantity is why practitioners can compare one result against another over time.
Eight virulence-factor genes
babA cagA dupA iceA oipA vacA virB virD
Whether the strain present carries each of these genes. Some H. pylori strains carry them and some do not.
Resistance-associated markers
clarithromycin- and fluoroquinolone-associated
Whether genetic markers associated with resistance to those drug classes were detected.
Swipe the table sideways to see every column →

Virulence factor explorer

The eight virulence factors, one at a time

Tap a gene to see what the abbreviation stands for and what kind of factor it is.

cagA — cytotoxin-associated gene A

The most extensively studied of the group. It sits within a larger genetic region and is delivered into host cells by a bacterial secretion system.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

vacA — vacuolating cytotoxin A

A secreted toxin. It exists in several allele types, which is part of why laboratories report it specifically rather than as a simple present/absent.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

babA — blood group antigen-binding adhesin A

An adhesin — a surface protein involved in attaching to the stomach lining.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

oipA — outer inflammatory protein A

An outer-membrane protein.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

dupA — duodenal ulcer-promoting gene A

The name reflects the clinical context in which it was first described in the research literature. A gene name is not a prediction about an individual, and its presence on your report does not forecast your course.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

iceA — “induced by contact with epithelium” gene A

Named because its expression was observed to increase on contact with epithelial cells.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

virB — type IV secretion system component

Part of the apparatus bacteria use to deliver molecules into host cells.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

virD — type IV secretion system component

Also associated with that delivery apparatus.

What it does not decide: whether you are treated, or with what. Detecting a virulence-factor gene is one input a clinician may weigh alongside your symptoms and history. The panel reports the genotype; it does not prescribe.

These are the names and functional classes of the genes reported. This page does not assign a clinical outcome to any individual gene, because that requires the kind of evidence review we are not prepared to shortcut.

What virulence factors are — and what they are not

A virulence factor is a gene whose product helps a bacterium establish itself or damage host tissue. Not every H. pylori strain carries the same set, which is the reason for testing them: two people can both "have H. pylori" and be carrying genetically different strains. cagA and vacA are the two most extensively studied.

Here is the part most pages will not tell you plainly. Detecting a virulence-factor gene does not, on its own, determine what should happen next. It is one input a clinician may weigh alongside your symptoms, your history, your family history and current clinical guidance. The panel reports the genotype; it does not prescribe, and neither do we. If a site tells you a particular gene means you must take a particular treatment, that is going further than a laboratory result can support.

Resistance markers vs a susceptibility test

These are related but genuinely different things, and conflating them causes real problems. A resistance-associated genetic marker is a sequence found in the sample that is associated with resistance. A susceptibility test grows the organism and measures whether a specific drug actually inhibits it. The first is faster and possible from stool; the second is the direct measurement.

Practically: a resistance marker is useful information for the clinician choosing a regimen, and it is not a substitute for their judgement or for culture-based testing where that is indicated.

Before you collect the sample

Tell the practitioner reviewing your intake what you are taking. Proton-pump inhibitors, antibiotics and bismuth-containing products can all influence H. pylori testing, and the practitioner needs to know in order to interpret the result or advise on timing. Do not stop a prescribed medication on your own to take a test — ask the prescriber first.

If H. pylori is detected

Take the report to a clinician who can manage it. Eradication is a prescription regimen, decisions about confirming eradication afterwards are clinical, and neither is something a stool panel or a wellness protocol settles. H. pylori is one of the findings on this panel where the honest advice is genuinely "see a doctor about this", and we would rather say so than sell you a supplement.

H. pylori with virulence factors and resistance markers — on the full panel, or on its own.

H. Pylori Profile — $237 → Full panel — $525

Medically reviewed by

Madison Ordway, FDN-P

Functional Diagnostic Nutrition Practitioner specializing in gut health, hormone balance and mineral optimization. Madison uses GI-MAP testing in her work with clients and has been featured in US Insider, Women’s Journal and The Science Times. See press features →

Content reviewed against Diagnostic Solutions Laboratory documentation and peer-reviewed literature. Last reviewed 24 July 2026.

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