Identify the toxin that is released by Helicobacter pylori in peptic ulcer?

RIMS Nursing Officer - 2022

Applied Microbiology & Infection control

Easy

Appeared in: RIMS Nursing Officer - 2022

Explanation

The correct option identifies the two primary toxins produced by H. pylori that are responsible for gastric mucosal damage.
VacA (Vacuolating cytotoxin A) is a secreted toxin that induces vacuolation (formation of large vacuoles) and apoptosis (programmed cell death) in gastric epithelial cells.
CagA (Cytotoxin-associated gene A) is a protein injected into host cells via a type IV secretion system. It disrupts cellular signaling pathways, leading to increased inflammation, cell proliferation, and a higher risk of peptic ulcers and gastric cancer.
Strains of H. pylori that express both CagA and VacA are considered highly virulent and are strongly associated with severe gastroduodenal diseases.

Option A: COX-1 (Cyclooxygenase-1) is a host enzyme, not a bacterial toxin. It plays a protective role in the gastric mucosa by synthesizing prostaglandins.
Option B: XagA/XavB are not recognized virulence factors or toxins produced by H. pylori. They are fictional names used as distractors.
Option D: FagB/FavB are not recognized virulence factors or toxins produced by H. pylori. They are fictional names used as distractors.

Clinical Relevance

Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Pathophysiology of H. pylori infection and its role in peptic ulcer disease as background academic context rather than a clinical decision trigger.
Understanding the role of CagA and VacA is crucial because testing for CagA-positive strains of H. pylori can help stratify a patient's risk for more severe outcomes, such as gastric adenocarcinoma.
Nurses play a key role in educating patients about the importance of completing the full course of H. pylori eradication therapy (which typically includes antibiotics and a proton pump inhibitor) to prevent recurrence of ulcers and reduce long-term cancer risk.
What if the patient is asymptomatic but tests positive for a CagA-positive H. pylori strain? In some cases, especially with a family history of gastric cancer, physicians may still recommend eradication therapy to mitigate future risk, and nursing support for treatment adherence is vital.

How to Approach the Question

First, identify the key components of the question: it asks for a 'toxin' released by 'Helicobacter pylori' in the context of 'peptic ulcer'.
Scan the options to see if any are familiar from the study of microbiology and gastroenterology.
Recall or deduce the major virulence factors of H. pylori. The most well-known are Urease, CagA, and VacA.
Evaluate Option A: COX-1. Recognize this as a human enzyme related to prostaglandin synthesis and NSAID-induced ulcers, not a bacterial toxin. Eliminate it.
Evaluate Options B and D: XagA/XavB and FagB/FavB. These names do not correspond to known major virulence factors and are likely distractors.
Evaluate Option C: CagA/VacA. These are the two most prominent toxins associated with H. pylori-induced cell damage and ulceration. This aligns with the core knowledge of the topic.

Concept Tested & Keywords

Concept Tested: Pathophysiology of H. pylori infection and its role in peptic ulcer disease.
Stem keywords: toxin, Helicobacter pylori, peptic ulcer
Lead-in keywords: Identify
Negative lead-in flag: false

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E6 Medicine Harrison 22e Part 2 p. 424-426

E6 Medicine Davidson Principles Practice 24e p. 818-820