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首页> 外文期刊>Journal of Clinical Microbiology >Molecular Characterization of an Epidemic Clone of Panantibiotic-Resistant Pseudomonas aeruginosa
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Molecular Characterization of an Epidemic Clone of Panantibiotic-Resistant Pseudomonas aeruginosa

机译:耐全抗生素的铜绿假单胞菌流行性克隆的分子表征

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We describe the molecular characterization of a multiresistant Pseudomonas aeruginosa clone causing an outbreak in the intensive care unit (ICU) of a tertiary-care university hospital. Analysis included antimicrobial susceptibility profile, O-serotyping, pulsed-field gel electrophoresis, and amplified fragment length polymorphism. Resistance mechanisms were characterized, including production of naturally occurring and acquired β-lactamases, porin expression, and efflux pump systems. Eighteen patients were colonized or infected with multiresistant P. aeruginosa. Multiresistant P. aeruginosa was panresistant to penicillins, cephalosporins, carbapenems, aminoglycosides, and fluoroquinolones and remained susceptible only to colistin. Sixteen isolates (89%) belonged to serotype O:11, pulsed-field gel electrophoresis type A1, and amplified fragment length polymorphism type A. Resistance characterization of this epidemic clone showed an overexpression of the chromosomal cephalosporinase AmpC combined with decreased expression of porin OprD and the absence of metallo-β-lactamase or extended-spectrum beta-lactamase. An upregulation of the MexXY efflux system due to an agrZ mutation in the mexZ repressor was detected. This epidemic clone was restricted to the ICU and was not found elsewhere in hospital. Contamination of the ICU environment and the hands of an ICU nurse with this clone suggests possible hand-borne transmission. Implementation of contact precautions effectively controlled transmission of the epidemic clone. This study illustrates the ability of multiresistant P. aeruginosa to cause an outbreak with significant morbidity and mortality and underscores the need to identify clonal outbreaks, which require targeted infection control measures.
机译:我们描述了引起三级护理大学医院的重症监护病房(ICU)暴发的多重耐药性铜绿假单胞菌克隆的分子特征。分析包括抗菌药物敏感性分布,O型分型,脉冲场凝胶电泳和扩增的片段长度多态性。耐药机制的特征包括自然产生的和获得性的β-内酰胺酶的产生,孔蛋白表达和外排泵系统。 18名患者被定植或感染了多药耐药性 P。铜绿。多抗性 P。铜绿假单胞菌对青霉素,头孢菌素,碳青霉烯类,氨基糖苷类和氟喹诺酮类药物具有全抗性,并且仅对粘菌素敏感。 16个分离株(占89%)属于血清型O:11,脉冲场凝胶电泳A1型和扩增的片段长度多态性A型。该流行性克隆的抗性表征显示染色体头孢菌素酶AmpC的过表达与孔蛋白OprD的表达降低相结合。并且没有金属β-内酰胺酶或广谱β-内酰胺酶。检测到由于 mexZ 阻遏物中的 agrZ 突变而导致的MexXY外排系统上调。该流行病克隆仅限于ICU,在医院其他地方未发现。该克隆感染了ICU环境和ICU护士的手,表明可能通过手传播。接触预防措施的实施有效地控制了流行性克隆的传播。这项研究说明了多抗性 P的能力。铜绿假单胞菌会引起高发病率和高死亡率的暴发,并强调需要确定克隆性暴发,这需要有针对性的感染控制措施。

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