Tsakris Athanassios, Ikonomidis Alexandros, Poulou Aggeliki, Spanakis Nicholas, Pournaras Spyros, Markou Fani
Department of Microbiology, Medical School, University of Athens, Athens, Greece.
J Antimicrob Chemother. 2007 Jul;60(1):136-9. doi: 10.1093/jac/dkm138. Epub 2007 May 8.
Several infections among patients attending our outpatient clinic were caused by imipenem-resistant Proteus mirabilis that were phenotypically metallo-beta-lactamase (MBL)-positive. The aim of the study was to investigate this extrahospital dissemination and the mechanisms of resistance to carbapenems.
During a 1 year period (December 2005-December 2006), the characteristics of the outpatients with infections caused by isolates of P. mirabilis with reduced susceptibility to imipenem (MIC > 4 mg/L) were prospectively collected. The isolates were tested by agar dilution MICs, phenotypic MBL testing and enterobacterial repetitive intergenic consensus PCR. PCR assays and nucleotide sequencing were used for the identification of bla gene types and mapping of the integron carrying the MBL gene. The location of the MBL allele was investigated by mating experiments, plasmid analysis and hybridization of the Southern-blotted plasmid extract with a bla(VIM-1) probe.
During the study, 12 MBL-positive P. mirabilis isolates were recovered from urinary tract infections of community patients. In all cases, the patients had a previous hospitalization in a Greek regional hospital and had received fluoroquinolones and/or aminoglycosides and beta-lactams. MICs of imipenem ranged from 32 to >128 mg/L, whereas those of meropenem ranged from 1 to 8 mg/L and those of ertapenem ranged from 0.5 to 4 mg/L. The isolates originated from the same clonal strain and harboured a bla(VIM-1) gene in a common integron structure. Conjugation experiments, plasmid analysis and hybridization assays indicated the chromosomal location of the bla(VIM-1) gene.
This is the first study that documents transmission in the extrahospital setting of acquired MBL-producing Gram-negatives causing community-onset infections.
在我们门诊就诊的患者中,有几例感染是由对亚胺培南耐药的奇异变形杆菌引起的,这些菌株表型上为金属β-内酰胺酶(MBL)阳性。本研究的目的是调查这种医院外传播情况以及对碳青霉烯类抗生素的耐药机制。
在1年期间(2005年12月至2006年12月),前瞻性收集了由对亚胺培南敏感性降低(MIC>4mg/L)的奇异变形杆菌分离株引起感染的门诊患者的特征。通过琼脂稀释法测定MIC、进行表型MBL检测以及肠杆菌重复基因间共有序列PCR对分离株进行检测。采用PCR检测和核苷酸测序来鉴定bla基因类型并对携带MBL基因的整合子进行定位。通过接合试验、质粒分析以及用bla(VIM-1)探针与Southern印迹质粒提取物杂交来研究MBL等位基因的位置。
在研究期间,从社区患者的尿路感染中分离出12株MBL阳性奇异变形杆菌。所有病例中,患者此前均在希腊一家地区医院住院治疗,并接受过氟喹诺酮类和/或氨基糖苷类以及β-内酰胺类药物治疗。亚胺培南的MIC范围为32至>128mg/L,美罗培南的MIC范围为1至8mg/L,厄他培南的MIC范围为0.5至4mg/L。这些分离株源自同一克隆菌株,并且在一个共同的整合子结构中携带bla(VIM-1)基因。接合试验、质粒分析和杂交检测表明bla(VIM-1)基因位于染色体上。
这是第一项记录在医院外环境中获得性产MBL革兰阴性菌引起社区发病感染传播情况的研究。