Department of Infection Control, Amphia Hospital, Breda, the Netherlands.
Laboratory for Medical Microbiology and Immunology, Elisabeth-TweeSteden Hospital, Tilburg, the Netherlands.
Antimicrob Resist Infect Control. 2020 Mar 16;9(1):48. doi: 10.1186/s13756-020-00708-7.
To determine the effect of exposure to remnants of a phagemid-containing E. coli, killed by treatment with a propanol-based hand rub, on antimicrobial resistance in E. coli isolates.
An in vitro model was developed in which a clinical E. coli isolate (EUR1) was exposed to remnants of an E. coli K-12 strain containing a phagemid (pBS-E12) strain treated with Sterillium®. A series of 200 experiments was performed using this in vitro model. As a control, a series of 400 experiments was performed where the EUR1 was exposed either to the remnants of an E. coli K-12 strain (not containing a phagemid) (E12) treated with Sterillium® (n = 200) or to dried Sterillium® only (n = 200). The number of experiments that showed growth of an amoxicillin-resistant EUR1 isolate was evaluated in all three groups. An additional 48 experiments were performed in which a different clinical E. coli isolate (EUR2) was exposed to remnants of the pBS-E12 treated with Sterillium®. Whole-genome sequencing and phenotypic testing for AmpC beta-lactamase production was performed to investigate the mechanism behind this resistance development.
In 22 (11.0%) of 200 experiments in which the EUR1 isolate was exposed to remnants of a pBS-E12 an amoxicillin-resistant mutant isolate was obtained, as opposed to only 2 (1.0%) of 200 experiments involving the exposure of the EUR1 to Sterillium® only (risk difference: 10.0%; 95% CI 5.4-14.6%)) and 1 (0.5%) of 200 experiments involving the exposure of the EUR1 isolate to the remnants of the phagemid-free E12 (risk difference: 10.5%; 95% CI 6.1-14.9%). In 1 (2.1%) of the 48 experiments in which the EUR2 isolate was exposed to remnants of a pBS-E12 an amoxicillin-resistant mutant isolate was obtained. The development of resistance in all experiments was due to mutations in the promoter/attenuator region of the chromosomal AmpC beta-lactamase (cAmpC) gene leading to cAmpC hyperproduction.
Exposure of an E. coli isolate to another phagemid-containing E. coli that was treated with propanol-based hand rub increased the development of amoxicillin resistance. Although phagemids are cloning vectors that are not present in clinical isolates, this finding may have implications for hand disinfection practices in healthcare facilities.
确定接触经丙醇基手部消毒剂处理过的含噬菌体质粒的大肠杆菌残留物对大肠杆菌分离株的抗菌药物耐药性的影响。
建立了一个体外模型，其中临床大肠杆菌分离株（EUR1）接触经 Sterillium 处理的含有噬菌体质粒（pBS-E12）的大肠杆菌 K-12 菌株的残留物。使用该体外模型进行了一系列 200 次实验。作为对照，进行了一系列 400 次实验，其中 EUR1 分别接触经 Sterillium 处理的不含噬菌体质粒的大肠杆菌 K-12 菌株（E12）（n=200）或仅接触干燥的 Sterillium（n=200）。评估了三组中所有实验中显示出耐阿莫西林的 EUR1 分离株生长的实验数量。另外进行了 48 次实验，其中不同的临床大肠杆菌分离株（EUR2）接触经 Sterillium 处理的 pBS-E12 的残留物。进行全基因组测序和表型测试以检测 AmpC 内酰胺酶产生，以研究这种耐药性发展的机制。
在 200 次 EUR1 分离株接触 pBS-E12 残留物的实验中，有 22 次（11.0%）获得了耐阿莫西林的突变株分离株，而仅在 200 次实验中接触 Sterillium 的实验中，有 2 次（1.0%）（风险差异：10.0%；95%CI 5.4-14.6%）和在 200 次 EUR1 分离株接触无噬菌体质粒的 E12 残留物的实验中，有 1 次（0.5%）（风险差异：10.5%；95%CI 6.1-14.9%）。在 48 次 EUR2 分离株接触 pBS-E12 残留物的实验中，有 1 次（2.1%）获得了耐阿莫西林的突变株分离株。所有实验中耐药性的发展是由于染色体 AmpC 内酰胺酶（cAmpC）基因的启动子/衰减子区域的突变导致 cAmpC 过度产生。
接触经丙醇基手部消毒剂处理过的含有另一种噬菌体质粒的大肠杆菌增加了耐阿莫西林的分离株的发展。尽管噬菌体质粒是不存在于临床分离株中的克隆载体，但这一发现可能对医疗机构的手部消毒实践产生影响。
