Department of Clinical Medicine, Trinity College Dublin, Ireland.
Aliment Pharmacol Ther. 2009 Oct;30(7):784-90. doi: 10.1111/j.1365-2036.2009.04095.x. Epub 2009 Jul 9.
Helicobacter pylori infection is eradicated with antimicrobial agents and drug-resistant strains make successful treatment difficult. Geographical variations in virulence-factor genotype also exist.
To evaluate prevalence of drug resistance and virulence-factor genotype in Irish H. pylori strains and to investigate if there is any relationship between drug resistance and genotype.
Helicobacter pylori strains isolated from 103 patients were examined. Antimicrobial susceptibilities were tested by Etest. The virulence-factor genotypes were determined using PCR. Frequencies of spontaneous metronidazole-resistance were measured in vitro.
Metronidazole resistance was present in 37.9% of strains examined. 16.5% of strains were clarithromycin-resistant and resistance to both agents observed was found in 12.6% of strains. 68% of strains were cagA(+). The dominant vacA type was s1/m2, followed by s1/m1 and s2/m2. The metronidazole resistance rate in cagA(-) group was significantly higher than in cagA(+) (P = 0.0089). Spontaneous resistance to metronidazole in cagA(-) occurred in higher frequency when compared with cagA(+).
cagA(+) and vacAs1/m2 type was the dominant genotype in Irish H. pylori strains. Significant rates of metronidazole resistance were observed in cagA(-) group. cagA(-) strains tend to acquire metronidazole resistance in vitro. Absence of cagA might be a risk factor in development of metronidazole resistance.
幽门螺杆菌感染可通过抗菌药物根除,但耐药菌株的出现使得治疗变得困难。此外,毒力因子基因型在地理上也存在差异。
评估爱尔兰幽门螺杆菌菌株的耐药性和毒力因子基因型的流行情况,并研究耐药性与基因型之间是否存在关系。
检测了 103 例患者分离的幽门螺杆菌菌株。采用 Etest 法检测抗菌药物敏感性,PCR 法检测毒力因子基因型,体外测量自发甲硝唑耐药率。
检测的菌株中,甲硝唑耐药率为 37.9%,克拉霉素耐药率为 16.5%,两种药物同时耐药率为 12.6%。68%的菌株为 cagA(+)。优势 vacA 型为 s1/m2,其次是 s1/m1 和 s2/m2。cagA(-)组的甲硝唑耐药率显著高于 cagA(+)组(P = 0.0089)。与 cagA(+)相比,cagA(-)菌株自发甲硝唑耐药的发生率更高。
爱尔兰幽门螺杆菌菌株中 cagA(+)和 vacAs1/m2 型是主要基因型。cagA(-)组观察到显著的甲硝唑耐药率。cagA(-)菌株在体外易获得甲硝唑耐药性。cagA 缺失可能是甲硝唑耐药发展的一个危险因素。