Hibbert-Rogers L C, Heritage J, Gascoyne-Binzi D M, Hawkey P M, Todd N, Lewis I J, Bailey C
Department of Microbiology, University of Leeds, UK.
J Antimicrob Chemother. 1995 Jul;36(1):65-82. doi: 10.1093/jac/36.1.65.
Between the autumn of 1989 and January 1990, 21 of the 44 children on the paediatric oncology ward of St. James's University Hospital, Leeds, UK were infected or colonised with Enterobacteriaceae producing extended-spectrum beta-lactamases. This represents 48% of the patients on the ward. Only six patients (14%) had microbiologically proven septicaemia caused by such bacteria during this period. Eighty-one isolates of Enterobacteriaceae producing extended-spectrum beta-lactamases derived from blood culture (7 isolates from 6 patients) or faecal samples (74 isolates) were available for examination. These comprised 28 Escherichia coli, 28 Klebsiella oxytoca, 11 Klebsiella pneumoniae, 10 Citrobacter freundii, 3 Enterobacter spp. and 1 Serratia marcescens. Clinical isolates were resistant to penicillins and to ceftazidime. Strains isolated in this study also showed multiple resistance to a range of antimicrobial agents. Transfer to a nalidixic acid resistant laboratory strain of E. coli UB5201 was attempted, but transfer of the ceftazidime resistance determinant was only successful in 25 isolates (31%). Examination of plasmid DNA revealed sequences in each isolate that hybridised with the TEM beta-lactamase gene probe used on a variety of plasmids ranging in size from 2.5- > 150 kb, sometimes found on several replicons in a single isolate. The TEM gene probe also hybridised with chromosomal DNA in a large number of isolates. Nucleotide sequence analysis demonstrated the presence of three extended-spectrum beta-lactamases: TEM-10B produced by two isolates, TEM-12B produced by 37 isolates and TEM-26B produced by 40 isolates. In two cases, isolates produced two beta-lactamases, and it proved impossible to identify these enzymes unequivocally. The genes encoding TEM-10B and TEM-26B both differ from TEM-12B by single nucleotide substitutions. Analysis of the ribotype patterns derived from the clinical isolates provided evidence for cross-colonisation between patients, and this was confirmed by analysis of the plasmid profiles. Four years after discontinuing ceftazidime and other extended-spectrum cephalosporins on this ward, patients were still colonised with bacteria that produced extended-spectrum beta-lactamases.
1989年秋至1990年1月期间，英国利兹圣詹姆斯大学医院儿科肿瘤病房的44名儿童中，有21名感染了产超广谱β-内酰胺酶的肠杆菌科细菌或被其定植。这占该病房患者的48%。在此期间，只有6名患者（14%）经微生物学证实由这类细菌引起败血症。从血培养（6名患者的7株）或粪便样本（74株）中获得了81株产超广谱β-内酰胺酶的肠杆菌科细菌分离株用于检测。这些分离株包括28株大肠埃希菌、28株产酸克雷伯菌、11株肺炎克雷伯菌、10株弗氏柠檬酸杆菌、3株肠杆菌属细菌和1株黏质沙雷菌。临床分离株对青霉素和头孢他啶耐药。本研究中分离出的菌株还对一系列抗菌药物表现出多重耐药。尝试将耐药性转移至耐萘啶酸的大肠埃希菌实验室菌株UB5201，但头孢他啶耐药决定簇仅在25株分离株（31%）中成功转移。对质粒DNA的检测显示，每个分离株中都有与TEMβ-内酰胺酶基因探针杂交的序列，该探针可用于多种大小从2.5至大于150 kb的质粒，有时在单个分离株的多个复制子上发现。TEM基因探针也与大量分离株的染色体DNA杂交。核苷酸序列分析表明存在三种超广谱β-内酰胺酶：2株分离株产生TEM-10B，37株分离株产生TEM-12B，40株分离株产生TEM-26B。在两例中，分离株产生两种β-内酰胺酶，且无法明确鉴定这些酶。编码TEM-10B和TEM-26B的基因与TEM-12B均仅存在单核苷酸替换差异。对临床分离株的核糖体分型模式分析为患者之间的交叉定植提供了证据，质粒图谱分析也证实了这一点。在该病房停用头孢他啶和其他超广谱头孢菌素四年后，患者仍被产超广谱β-内酰胺酶的细菌定植。
