Related Experiment Video

Updated: Oct 17, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

Factors associated with Helicobacter pylori infection by a cagA-positive strain in children

D M Queiroz1, E N Mendes, A S Carvalho

  • 1Laboratory of Research in Bacteriology, Faculdade de Medicina/UFMG, 30130-100, Belo Horizonte, MG, Brazil. dqueiroz@medicina.ufmg.br

The Journal of Infectious Diseases
|February 11, 2000
PubMed

Insights

Helicobacter pylori cagA-positive strains are linked to duodenal ulcers in children. This cagA status also correlates with more severe gastritis and older age in pediatric patients.

Area of Science:

  • Pediatric Gastroenterology
  • Microbiology
  • Molecular Diagnostics

Background:

  • Helicobacter pylori infection is a known risk factor for duodenal peptic ulcers in adults.
  • The association between cagA-positive H. pylori strains and duodenal ulcers in children remains under-investigated.

Purpose of the Study:

  • To investigate the association between cagA-positive H. pylori strains and duodenal ulcer disease in a pediatric cohort.
  • To evaluate the relationship between cagA status and the severity of gastritis in children.

Main Methods:

  • Polymerase chain reaction (PCR) was used to detect the cagA gene in H. pylori strains.
  • H. pylori strains were isolated from children with and without duodenal ulcers.
  • Gastric mucosal biopsies were analyzed for gastritis severity and inflammatory cell infiltration.

Main Results:

  • A significantly higher prevalence of cagA-positive H. pylori was observed in children with duodenal ulcers (100%) compared to those without (62.3%) (P=.00007).
  • cagA-positive status was associated with more severe macroscopic gastritis, increased inflammatory infiltrate, and mucosal degenerative/regenerative changes.
  • Increased cagA positivity correlated with older age in the pediatric study group.

Conclusions:

  • The cagA-positive status of H. pylori is strongly associated with duodenal ulcer disease in children.
  • cagA-positive H. pylori infection contributes to more severe gastric inflammation and mucosal damage in pediatric patients.
  • Age is a factor associated with cagA positivity in children with H. pylori infection.

More Related Videos

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.