Klesiewicz Karolina, Orczykowska-Kotyna Monika, Skiba-Kurek Iwona, Empel Joanna, Kania Katarzyna, Karczewska Elżbieta
Department of Pharmaceutical Microbiology, Faculty of Pharmacy, Jagiellonian University Medical College, 9 Medyczna Street, Krakow, 30-688, Poland.
Department of Epidemiology and Clinical Microbiology, National Medicines Institute, 30/34 Chełmska Street, Warsaw, 00-725, Poland.
Eur J Clin Microbiol Infect Dis. 2025 Feb;44(2):405-416. doi: 10.1007/s10096-024-05018-z. Epub 2024 Dec 17.
Assessment of Helicobacter pylori (H. pylori) prevalence in Southern Poland, focusing on highly virulent cagA-positive strains associated with gastric cancer risk, along with analysis of antimicrobial resistance and its molecular mechanisms.
A total of 130 dyspeptic patients, who underwent endoscopy, were enrolled in the study. Presence of H. pylori in gastric mucosa biopsy specimens was confirmed by rapid urease tests, histological examination, culture, and molecular assays. Antimicrobial susceptibility was tested using the E-test, while the cagA gene (virulence marker) was identified by PCR. The GenoType HelicoDR detected mutations for resistance to clarithromycin (23 S rRNA) and levofloxacin (gyrA). Resistance to rifampicin and levofloxacin was investigated by sequencing the rpoB and gyrA genes.
H. pylori prevalence in Southern Poland was 30.8%, with 60% of infections involving cagA-positive strains. Susceptibility testing revealed resistance rates of 22.9% for metronidazole, 14.3% for clarithromycin, 11.4% for levofloxacin and 25.7% for rifampicin. Among the 24 cagA-positive strains, 45.8% were resistant to at least one antibiotic. Clarithromycin resistance was caused by A2143G mutation. The gyrA gene sequence showed the N87K mutation linked to fluoroquinolone resistance. No mutations were found in the rpoB gene.
Infections with multidrug-resistant CagA-positive strains require recommended treatment strategies due to the high risk of progression of infection to gastric cancer.
评估波兰南部幽门螺杆菌（H. pylori）的流行情况，重点关注与胃癌风险相关的高毒力cagA阳性菌株，并分析其耐药性及其分子机制。
共有130例接受内镜检查的消化不良患者纳入本研究。通过快速尿素酶试验、组织学检查、培养和分子检测确认胃黏膜活检标本中是否存在幽门螺杆菌。使用E-test检测抗菌药物敏感性，同时通过PCR鉴定cagA基因（毒力标志物）。GenoType HelicoDR检测对克拉霉素（23 S rRNA）和左氧氟沙星（gyrA）耐药的突变。通过对rpoB和gyrA基因进行测序研究对利福平和左氧氟沙星的耐药性。
波兰南部幽门螺杆菌感染率为30.8%，其中60%的感染涉及cagA阳性菌株。药敏试验显示甲硝唑耐药率为22.9%，克拉霉素为14.3%，左氧氟沙星为11.4%，利福平为25.7%。在24株cagA阳性菌株中，45.8%对至少一种抗生素耐药。克拉霉素耐药是由A2143G突变引起。gyrA基因序列显示N87K突变与氟喹诺酮耐药有关。rpoB基因未发现突变。
由于多重耐药的CagA阳性菌株感染进展为胃癌的风险很高，因此需要推荐的治疗策略。
