Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Anesthesia and Surgical Intensive Care Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
J Med Microbiol. 2021 Oct;70(10). doi: 10.1099/jmm.0.001432.
The resistance to quinolone reported in uropathogenic (UPEC) is commonly caused by mutations in the target site encoding genes such as the gene. Bacterial plasmids carrying resistance genes such as genes can also transfer resistance. Biofilms produced by UPEC can further aid the development of resistant urinary tract infections (UTIs). Biofilm production is associated with higher prevalence of quinolones resistance genetic determinants. To detect the prevalence of genes and gene mutation among quinolone-resistant UPEC and to investigate the relation between these genetic resistance determinants and biofilm production. Catheterized urine samples were collected from 420 patients with evidence of UTIs and processed using standard techniques. Isolated UPEC were screened for quinolone resistance using an antimicrobial susceptibility test. Biofilm production among quinolone-resistant isolates was detected using the tissue culture plate method. All quinolone-resistant isolates were screened for genes ( and ) by multiplex PCR and for gene mutation by PCR-RFLP. Two hundred and sixty-four UPEC isolates were detected from 420 processed urine samples. Out of the identified 264 UPEC 123 (46.6 %) isolates were found to be quinolone-resistant, showing resistance to 1 or more of the tested quinolones. Of the 123 quinolone-resistant UPEC detected, 71(57.7 %) were biofilm producers. The genes were detected among 62.6 % of the quinolone-resistant UPEC, with an estimated prevalence of 22.8 32.5 and 37.4 % for and genes, respectively. Additionally, the gene mutation was identified among 53.7 % of the quinolone-resistant isolates. We reported a significant association between biofilm production and the presence of , and genes. Furthermore, the gene mutation was significantly associated with biofilm-producing isolates. The coexistence of genes, gene mutation and biofilm production was demonstrated in almost 40 % of the quinolone-resistant isolates. A significantly higher prevalence of genes ( and ) as well as the gene mutation was found among biofilm-forming UPEC. The reported coexistence of these different resistance mechanisms could aggravate quinolone resistance. Therefore, monitoring of resistance mechanisms and a proper stewardship programme are necessary.
尿路感染（UPEC）中报告的对喹诺酮类药物的耐药性通常是由靶位编码基因突变引起的，例如 基因。携带耐药基因（如 基因）的细菌质粒也可以转移耐药性。UPEC 产生的生物膜可以进一步帮助发展耐药性尿路感染（UTI）。生物膜的产生与更高的喹诺酮耐药遗传决定因素的流行有关。为了检测喹诺酮类耐药 UPEC 中 基因和 基因突变的流行情况，并探讨这些遗传耐药决定因素与生物膜产生之间的关系。从 420 名有 UTI 证据的患者中收集导尿管尿液样本，并使用标准技术进行处理。使用抗菌药物敏感性试验筛选分离的 UPEC 对喹诺酮类药物的耐药性。使用组织培养板法检测喹诺酮类耐药分离株的生物膜产生情况。使用多重 PCR 筛选所有喹诺酮类耐药分离株的 基因（和 ），并使用 PCR-RFLP 筛选 基因突变。从 420 份处理后的尿液样本中检测到 264 株 UPEC。在鉴定的 264 株 UPEC 中，有 123 株（46.6%）被发现对喹诺酮类药物耐药，对 1 种或多种测试的喹诺酮类药物耐药。在检测到的 123 株喹诺酮类耐药 UPEC 中，有 71 株（57.7%）为生物膜生产者。在喹诺酮类耐药 UPEC 中检测到 基因，估计 基因、 基因和 基因的流行率分别为 22.8%、32.5%和 37.4%。此外，在 53.7%的喹诺酮类耐药分离株中发现了 基因突变。我们报告了生物膜产生与 基因、 基因和 基因存在之间的显著相关性。此外， 基因突变与生物膜产生分离株显著相关。在几乎 40%的喹诺酮类耐药分离株中证实了 基因、 基因突变和生物膜产生的共存。在形成生物膜的 UPEC 中，发现 基因（和 ）以及 基因突变的流行率显著更高。报告的这些不同耐药机制的共存可能会加重喹诺酮类耐药性。因此，有必要监测耐药机制和适当的管理计划。
