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首页> 外文期刊>Journal of Clinical Microbiology >Outbreak of Dysentery Associated with Ceftriaxone-Resistant Shigella sonnei: First Report of Plasmid-Mediated CMY-2-Type AmpC β-Lactamase Resistance in S. sonnei
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Outbreak of Dysentery Associated with Ceftriaxone-Resistant Shigella sonnei: First Report of Plasmid-Mediated CMY-2-Type AmpC β-Lactamase Resistance in S. sonnei

机译:与耐头孢曲松的痢疾志贺氏菌相关的痢疾的爆发:沙门氏菌中质粒介导的CMY-2-型AmpCβ-内酰胺酶抗性的首次报道。

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摘要

We document the first report of plasmid-encoded CMY-2-type AmpC β-lactamase identified among Shigella sonnei isolates resistant to ceftriaxone and obtained after an outbreak of bacillary dysentery in Taiwan. One hundred eighty-two children in two elementary schools in Yu-Li, Taiwan, where an outbreak occurred after a typhoon hit this area in 2001, were enrolled in this study. Clinical and epidemiologic data on the infected children were collected. Pulsed-field gel electrophoresis (PFGE) was performed on the isolates to determine the genetic relatedness of outbreak strains. Plasmid analysis and PCR were performed to identify β-lactamase genes responsible for ceftriaxone resistance. Forty-seven children from the two elementary schools were culture positive for S. sonnei in this outbreak. Twenty-three children were asymptomatic. Of the total isolates 55.3% were resistant to ampicillin. One hundred percent of the isolates obtained from children in school A were initially susceptible to both ampicillin and ceftriaxone. Of isolates obtained from school B 96.2% were nonsusceptible to ceftriaxone. However, two isolates from school A developed resistance to ampicillin during the course of treatment. All 18 available isolates showed closely related PFGE patterns (4, 4a, 4b, and 4c). CMY-2-type AmpC β-lactamase was responsible for ceftriaxone resistance in ceftriaxone-nonsusceptible isolates; Southern blot hybridization confirmed that such a resistance gene was located on the plasmid. This is the first report of plasmid-mediated CMY-2-type AmpC β-lactamase in S. sonnei. Ampicillin-resistant isolates can develop during the course of antibiotic treatment.
机译:我们记录了首个报道的质粒编码的CMY-2-型AmpCβ-内酰胺酶,该菌株在台湾的细菌性痢疾暴发后对头孢曲松耐药的志贺氏志贺氏菌分离物中鉴定出。这项研究招募了台湾玉丽两所小学的一百八十二名儿童,该儿童在2001年台风袭击该地区后爆发。收集了有关受感染儿童的临床和流行病学数据。对分离株进行脉冲场凝胶电泳(PFGE),以确定爆发菌株的遗传相关性。进行质粒分析和PCR以鉴定引起头孢曲松抗性的β-内酰胺酶基因。两所小学的47名孩子对 S的文化呈阳性。这次爆发中的sonnei 。 23名儿童无症状。在所有分离株中,有55.3%对氨苄西林耐药。从学校A的孩子那里获得的分离株的100%最初对氨苄青霉素和头孢曲松均敏感。从学校B获得的分离株中96.2%对头孢曲松不敏感。但是,在治疗过程中,两名来自学校A的分离株对氨苄西林产生了耐药性。所有18种可用分离株均显示出密切相关的PFGE模式(4、4a,4b和4c)。 CMY-2型AmpCβ-内酰胺酶是导致头孢曲松敏感性不敏感菌株中头孢曲松耐药的原因。 Southern印迹杂交证实了这种抗性基因位于质粒上。这是 S中质粒介导的CMY-2-型AmpCβ-内酰胺酶的首次报道。 sonnei 。在抗生素治疗过程中会产生氨苄青霉素抗性分离株。

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