[Resistance to antibiotics used in Helicobacter pylori infection in children]

Elzbieta Maciorkowska1, Maciej Kaczmarski, Jarosław Kowalczuk

  • 1III Klinika Chorób Dzieci AM w Białymstoku. emaciorkowska@o2.pl

Insights

Antibiotic resistance in Helicobacter pylori is a growing concern, particularly for metronidazole and clarithromycin. This study found high rates of resistance in children, impacting eradication success.

Area of Science:

  • Microbiology
  • Pediatric Infectious Diseases
  • Pharmacology

Background:

  • Antibiotic resistance in Helicobacter pylori (H. pylori) is a significant clinical challenge, impacting the efficacy of eradication therapies.
  • Metronidazole and clarithromycin are key antibiotics used in H. pylori treatment, but resistance rates are increasing globally.
  • Understanding drug resistance patterns, especially in pediatric populations, is crucial for optimizing treatment strategies.

Purpose of the Study:

  • To evaluate primary and secondary drug resistance patterns of H. pylori in children undergoing eradication therapy.
  • To determine the prevalence of resistance to metronidazole, clarithromycin, amoxicillin, and tetracyclines in pediatric H. pylori infections.
  • To assess the impact of previous unsuccessful eradication attempts on antibiotic resistance.

Main Methods:

  • A study involving 50 children with H. pylori infections was conducted.
  • Drug resistance was assessed in children receiving initial eradication therapy and in 18 children with prior failed treatments.
  • Antimicrobial susceptibility testing was performed to determine resistance to key antibiotics.

Main Results:

  • High secondary resistance rates were observed for metronidazole (up to 72.0%) and macrolides (around 66.0%).
  • Primary resistance to clarithromycin was 25.0%, and combined primary resistance to clarithromycin and metronidazole was 7.2%.
  • No resistance to amoxicillin and tetracyclines was found in H. pylori isolates.

Conclusions:

  • Significant primary and secondary antibiotic resistance to metronidazole and clarithromycin exists in pediatric H. pylori infections.
  • The high resistance rates, especially secondary resistance, may explain treatment failures.
  • Amoxicillin and tetracyclines remain effective options, suggesting their potential role in salvage therapies.

Related Concept Videos

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 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...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
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...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current medication...