Eng R H, Yen K, Smith S M, Citron D M, Goldstein E J, Greenberg R, Cherubin C E
Infectious Disease Section, Department of Veterans Affairs, Medical Centers, East Orange, NJ 07018-1095.
Chemotherapy. 1992;38(6):399-404. doi: 10.1159/000239034.
Escherichia coli strains resistant to ampicillin/sulbactam from hospitals in 4 different geographic locations were examined with respect to type and amount of beta-lactamase produced. A total of 5 strains was examined from each region. The isoelectric points of all of the involved beta-lactamases were 5.4, corresponding to TEM-1. Km and Vmax values of the beta-lactamases among the clinical isolates resembled those from the control TEM-1 strain. In an 18-hour broth culture the highly resistant isolates produced 3 times more beta-lactamase as compared to the ampicillin/sulbactam-susceptible isolates. However, the highly resistant strains contained approximately the same amount of plasmid DNA (size of > 6,500 bp) as the susceptible isolates. In transformation experiments, both the resistance and the degree of resistance appeared to have been transferable by plasmids. The mechanism for resistance is likely to be a baseline overproduction of TEM-1 beta-lactamase due to either an alteration in the control of gene expression or simply to an increase in the number of copies of the beta-lactamase gene in the plasmids.
对来自4个不同地理位置医院的耐氨苄西林/舒巴坦的大肠杆菌菌株，就其产生的β-内酰胺酶类型和数量进行了检测。每个地区共检测了5株菌株。所有相关β-内酰胺酶的等电点均为5.4，与TEM-1相符。临床分离株中β-内酰胺酶的Km和Vmax值与对照TEM-1菌株相似。在18小时的肉汤培养中，高度耐药分离株产生的β-内酰胺酶比氨苄西林/舒巴坦敏感分离株多3倍。然而，高度耐药菌株所含的质粒DNA量（大小>6500 bp）与敏感分离株大致相同。在转化实验中，耐药性和耐药程度似乎都可通过质粒转移。耐药机制可能是由于基因表达控制的改变或仅仅是质粒中β-内酰胺酶基因拷贝数增加导致TEM-1β-内酰胺酶基线过量产生。
