Alvarez M, Tran J H, Chow N, Jacoby G A
Lahey Clinic, Burlington, and Edith Nourse Rogers Memorial Veterans Hospital, Bedford, Massachusetts, USA.
Antimicrob Agents Chemother. 2004 Feb;48(2):533-7. doi: 10.1128/AAC.48.2.533-537.2004.
A sample of 752 resistant Klebsiella pneumoniae, Klebsiella oxytoca, and Escherichia coli strains from 70 sites in 25 U.S. states and the District of Columbia was examined for transmissibility of resistance to ceftazidime and the nature of the plasmid-mediated beta-lactamase involved. Fifty-nine percent of the K. pneumoniae, 24% of the K. oxytoca, and 44% of the E. coli isolates transferred resistance to ceftazidime. Plasmids encoding AmpC-type beta-lactamase were found in 8.5% of the K. pneumoniae samples, 6.9% of the K. oxytoca samples, and 4% of the E. coli samples, at 20 of the 70 sites and in 10 of the 25 states. ACT-1 beta-lactamase was found at eight sites, four of which were near New York City, where the ACT-1 enzyme was first discovered; ACT-1 beta-lactamase was also found in Massachusetts, Pennsylvania, and Virginia. FOX-5 beta-lactamase was also found at eight sites, mainly in southeastern states but also in New York. Two E. coli strains produced CMY-2, and one K. pneumoniae strain produced DHA-1 beta-lactamase. Pulsed-field gel electrophoresis and plasmid analysis suggested that AmpC-mediated resistance spread both by strain and plasmid dissemination. All AmpC beta-lactamase-containing isolates were resistant to cefoxitin, but so were 11% of strains containing transmissible SHV- and TEM-type extended-spectrum beta-lactamases. A beta-lactamase inhibitor test was helpful in distinguishing the two types of resistance but was not definitive since 24% of clinical isolates producing AmpC beta-lactamase had a positive response to clavulanic acid. Coexistence of AmpC and extended-spectrum beta-lactamases was the main reason for these discrepancies. Plasmid-mediated AmpC-type enzymes are thus responsible for an appreciable fraction of resistance in clinical isolates of Klebsiella spp. and E. coli, are disseminated around the United States, and are not so easily distinguished from other enzymes that mediate resistance to oxyimino-beta-lactams.
对来自美国25个州及哥伦比亚特区70个地点的752株耐头孢他啶的肺炎克雷伯菌、产酸克雷伯菌和大肠杆菌菌株样本进行了耐药性传播及相关质粒介导的β-内酰胺酶性质的检测。59%的肺炎克雷伯菌、24%的产酸克雷伯菌和44%的大肠杆菌分离株可传递对头孢他啶的耐药性。在70个地点中的20个以及25个州中的10个，8.5%的肺炎克雷伯菌样本、6.9%的产酸克雷伯菌样本和4%的大肠杆菌样本中发现了编码AmpC型β-内酰胺酶的质粒。在8个地点发现了ACT-1β-内酰胺酶，其中4个地点靠近纽约市，ACT-1酶最初就是在那里发现的；在马萨诸塞州、宾夕法尼亚州和弗吉尼亚州也发现了ACT-1β-内酰胺酶。在8个地点也发现了FOX-5β-内酰胺酶，主要在东南部各州，但在纽约也有发现。2株大肠杆菌产生CMY-2，1株肺炎克雷伯菌产生DHA-1β-内酰胺酶。脉冲场凝胶电泳和质粒分析表明，AmpC介导的耐药性通过菌株和质粒传播。所有含AmpCβ-内酰胺酶的分离株对头孢西丁耐药，但含可传递的SHV型和TEM型超广谱β-内酰胺酶的菌株中也有11%耐药。β-内酰胺酶抑制剂试验有助于区分这两种耐药类型，但并不确定，因为24%产生AmpCβ-内酰胺酶的临床分离株对克拉维酸呈阳性反应。AmpC和超广谱β-内酰胺酶共存是这些差异的主要原因。因此，质粒介导的AmpC型酶在肺炎克雷伯菌和大肠杆菌临床分离株的耐药性中占相当比例，在美国各地传播，并且不容易与其他介导对氧亚氨基-β-内酰胺耐药的酶区分开来。
