MOLECULAR EPIDEMIOLOGY OF CEFTAZIDIME RESISTANT ENTEROBACTERIACEAE FROM PATIENTS ON A PEDIATRIC ONCOLOGY WARD
MOLECULAR EPIDEMIOLOGY OF CEFTAZIDIME RESISTANT ENTEROBACTERIACEAE FROM PATIENTS ON A PEDIATRIC ONCOLOGY WARD
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DOI：
10.1093/jac/36.1.65
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发表时间：
1995-07-01
影响因子：
5.2
通讯作者：
BAILEY, C
中科院分区：
文献类型：
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作者：
HIBBERTROGERS, LCF;HERITAGE, J;BAILEY, C
1989年秋至1990年1月，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名感染或定植了产超广谱β-内酰胺酶的肠杆菌科。这占病房病人的48%。在此期间，只有6名患者（14%）经微生物学证实由此类细菌引起的败血症。81株产超广谱β-内酰胺酶的肠杆菌科分离株来自血培养（6例患者的7株分离株）或粪便样本（74株分离株），可用于检查。其中包括28例大肠埃希菌、28例产酸克雷伯菌、11例肺炎克雷伯菌、10例弗氏柠檬酸杆菌、3例肠杆菌属和1例粘质沙雷菌。临床分离株对青霉素和头孢他啶耐药。本研究中分离的菌株对一系列抗菌药物也表现出多重耐药性。转移到耐萘啶酸的E.大肠杆菌UB 5201中，头孢他啶耐药决定簇的转移仅成功25株（31%）。质粒DNA的检查揭示了与TEM β-内酰胺酶基因探针杂交的每个分离株中的序列，所述探针用于大小从2 . 5->150 kb，有时在单个分离株的多个复制子上发现。TEM基因探针还与大量分离株中的染色体DNA杂交。核苷酸序列分析表明存在3种超广谱β-内酰胺酶：TEM-10 B由2株分离株产生，TEM-12 B由37株分离株产生，TEM-26 B由40株分离株产生。在两个病例中，分离株产生两种β-内酰胺酶，并且证明不可能明确鉴定这些酶。编码TEM-10 B和TEM-26 B的基因都与TEM-12 B的不同之处在于单核苷酸取代。来自临床分离株的核糖体型模式的分析提供了患者之间交叉定殖的证据，并且这通过质粒谱的分析得到证实。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。
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.