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Abstract：
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.
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.
摘要：
为了确定暴露于含有噬菌粒的大肠杆菌残留物的影响，用丙醇基手部摩擦处理杀死，大肠杆菌分离株的耐药性。
开发了体外模型,其中将临床大肠杆菌分离物(EUR1)暴露于含有用Sterillium®处理的噬菌粒(pBS-E12)菌株的大肠杆菌K-12菌株的残余物。使用该体外模型进行一系列200次实验。作为一种控制，进行了一系列的400个实验,其中将EUR1暴露于用Sterlium®(n=200)处理的大肠杆菌K-12菌株(E12)的残余物(不含有噬菌粒)或仅暴露于干燥的Sterlium®(n=200)。在所有三组中评估显示阿莫西林抗性EUR1分离株生长的实验数量。进行另外48个实验,其中将不同的临床大肠杆菌分离物(EUR2)暴露于用Sterlium®处理的pBS-E12的残余物。进行AmpCβ-内酰胺酶生产的全基因组测序和表型测试以研究这种抗性发展背后的机制。
在将EUR1分离物暴露于pBS-E12残留物的200个实验中的22个（11.0％）中，获得了耐阿莫西林的突变分离物，在涉及EUR1仅暴露于Sterillium®的200项实验中,仅有2项(1.0%)(风险差异:10.0%;95%CI5.4-14.6%)和涉及EUR1分离物暴露于不含噬菌粒的残留E12的200项实验中的1项(0.5%)(风险差异:10.5%;95%CI6.1-14.9%)。在将EUR2分离物暴露于pBS-E12残留物的48个实验中的1个（2.1％）中，获得了阿莫西林抗性突变分离物。在所有实验中，耐药性的发展是由于染色体AmpCβ-内酰胺酶（cAmpC）基因的启动子/衰减子区域的突变导致cAmpC高产量。
大肠杆菌分离物暴露于另一种用基于丙醇的手擦处理的含有噬菌粒的大肠杆菌增加了阿莫西林抗性的发展。尽管噬菌粒是临床分离物中不存在的克隆载体，这一发现可能会对医疗机构的手部消毒实践产生影响。
开发了体外模型,其中将临床大肠杆菌分离物(EUR1)暴露于含有用Sterillium®处理的噬菌粒(pBS-E12)菌株的大肠杆菌K-12菌株的残余物。使用该体外模型进行一系列200次实验。作为一种控制，进行了一系列的400个实验,其中将EUR1暴露于用Sterlium®(n=200)处理的大肠杆菌K-12菌株(E12)的残余物(不含有噬菌粒)或仅暴露于干燥的Sterlium®(n=200)。在所有三组中评估显示阿莫西林抗性EUR1分离株生长的实验数量。进行另外48个实验,其中将不同的临床大肠杆菌分离物(EUR2)暴露于用Sterlium®处理的pBS-E12的残余物。进行AmpCβ-内酰胺酶生产的全基因组测序和表型测试以研究这种抗性发展背后的机制。
在将EUR1分离物暴露于pBS-E12残留物的200个实验中的22个（11.0％）中，获得了耐阿莫西林的突变分离物，在涉及EUR1仅暴露于Sterillium®的200项实验中,仅有2项(1.0%)(风险差异:10.0%;95%CI5.4-14.6%)和涉及EUR1分离物暴露于不含噬菌粒的残留E12的200项实验中的1项(0.5%)(风险差异:10.5%;95%CI6.1-14.9%)。在将EUR2分离物暴露于pBS-E12残留物的48个实验中的1个（2.1％）中，获得了阿莫西林抗性突变分离物。在所有实验中，耐药性的发展是由于染色体AmpCβ-内酰胺酶（cAmpC）基因的启动子/衰减子区域的突变导致cAmpC高产量。
大肠杆菌分离物暴露于另一种用基于丙醇的手擦处理的含有噬菌粒的大肠杆菌增加了阿莫西林抗性的发展。尽管噬菌粒是临床分离物中不存在的克隆载体，这一发现可能会对医疗机构的手部消毒实践产生影响。
