Department of Microbiology and Immunology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa 252-0374, Japan.
J Med Microbiol. 2012 Dec;61(Pt 12):1727-1735. doi: 10.1099/jmm.0.049726-0. Epub 2012 Aug 30.
Proteus mirabilis is a common cause of urinary tract infection. Wild-type P. mirabilis strains are usually susceptible to penicillins and cephalosporins, but occurrences of P. mirabilis producing extended-spectrum β-lactamases (ESBLs) have been recently reported. Here, we surveyed the prevalence of cefotaxime resistance among P. mirabilis strains at seven different hospitals in Kanagawa Prefecture, Japan, and investigated their molecular epidemiology to explain the mechanism of their spread. The prevalence of cefotaxime resistance among P. mirabilis increased annually, from 10.1 % in 1998 to 23.1 % in 2003, and increased drastically in 2004, exceeding 40 %. We collected 105 consecutive and non-duplicate cefotaxime-resistant P. mirabilis isolates (MIC 16 to >256 µg ml(-1)) from these hospitals from June 2004 to May 2005 and characterized their profile. PCR and sequence analysis revealed that all resistant strains produced exclusively CTX-M-2 β-lactamase. PFGE analysis identified 47 banding patterns with 83 % or greater similarity. These results indicated that a regional outbreak of P. mirabilis producing CTX-M-2 β-lactamase has occurred in Japan and suggest that the epidemic spread occurred within and across hospitals and communities by extended clonal strains. Plasmid analysis revealed that 44.8 % of plasmids harboured by bla(CTX-M-2) isolates had common profiles, encoding ISEcp1, IS26 and Int1, and belonged to incompatibility group T. Spread of the resistant isolates in Japan resulted from dissemination of narrow-host-range plasmids of the IncT group encoding bla(CTX-M-2). These findings indicate the rapidly developing problem of treating the species to prevent dissemination of ESBL producers.
奇异变形杆菌是尿路感染的常见原因。野生型奇异变形杆菌通常对青霉素类和头孢菌素类敏感，但最近有报道称奇异变形杆菌产生超广谱β-内酰胺酶（ESBLs）。在这里，我们调查了日本神奈川县 7 家不同医院奇异变形杆菌对头孢噻肟耐药的流行情况，并对其分子流行病学进行了研究，以解释其传播机制。奇异变形杆菌对头孢噻肟的耐药率逐年上升，从 1998 年的 10.1%上升到 2003 年的 23.1%，2004 年急剧上升，超过 40%。我们从 2004 年 6 月至 2005 年 5 月从这些医院收集了 105 株连续的、非重复的头孢噻肟耐药奇异变形杆菌分离株（MIC16 至>256μg/ml），并对其特征进行了描述。PCR 和序列分析表明，所有耐药株均仅产生 CTX-M-2 型β-内酰胺酶。PFGE 分析鉴定出 47 种带型，相似度为 83%或更高。这些结果表明，日本发生了奇异变形杆菌产 CTX-M-2 型β-内酰胺酶的局部暴发，并表明流行通过扩展的克隆株在医院内和医院间以及社区内传播。质粒分析表明，bla(CTX-M-2)分离株携带的 44.8%的质粒具有共同的特征，编码 ISEcp1、IS26 和 Int1，并属于不相容群 T。耐药分离株在日本的传播是由于携带bla(CTX-M-2)的窄宿主范围质粒 IncT 组的传播。这些发现表明，治疗该物种以防止 ESBL 产生菌传播的问题正在迅速发展。
