Muratani Tetsuro, Kobayashi Tomoko, Matsumoto Tetsuro
Department of Urology, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Int J Antimicrob Agents. 2006 Jun;27(6):491-9. doi: 10.1016/j.ijantimicag.2006.03.007. Epub 2006 May 15.
Forty-six cephem-resistant Klebsiella pneumoniae strains with minimum inhibitory concentrations>8 microg/mL for cefpodoxime and cefmetazole were selected from clinical isolates obtained between 2000 and 2002 from eight hospitals on Northern Kyushu Island, Japan. We investigated the mechanisms of resistance to cephems in these 46 K. pneumoniae isolates. The results of isoelectric focusing of beta-lactamases produced by these isolates, polymerase chain reaction for detection of various Class A, Class B and Class C beta-lactamases, and determination of the sequence of the beta-lactamase structural gene showed that most of these isolates had various types of broad-spectrum beta-lactamases. Of the 46 isolates, 2 were CMY-2 beta-lactamase producers and 41 were DHA-1 beta-lactamase producers. Forty of the 41 DHA-1 beta-lactamase producers simultaneously produced SHV-12 extended-spectrum beta-lactamase (ESBL), and the remaining isolate simultaneously produced SHV-27. Furthermore, one DHA-1 and SHV-12 beta-lactamase producer also produced IMP-1 beta-lactamase. The only broad-spectrum beta-lactamase with another isolate was IMP-1. Chromosomal DNA restriction fragment analysis using XbaI suggested that nosocomial infection due to DHA-1 and SHV-12 beta-lactamase producers had occurred at two centres. This is the first report of nosocomial infection due to DHA-1 beta-lactamase-producing K. pneumoniae including other plasmid-encoded AmpC beta-lactamases in Japan. The mechanisms of resistance of 44 of the 46 isolates to cephalosporins and cephamycins were ESBL production and/or plasmid-encoded AmpC beta-lactamase and/or IMP-1 beta-lactamase production. For two isolates, the mechanism of resistance to could not be identified. These results show that it is necessary to minimise the prevalence of these resistant strains as it will be a very serious problem if organisms producing these broad-spectrum beta-lactamases increase in clinical situations. It is important to detect these strains sooner and to perform rigorous infection control earlier.
从2000年至2002年期间日本九州岛北部八家医院的临床分离株中，选取了46株对头孢泊肟和头孢美唑的最低抑菌浓度>8μg/mL的耐头孢菌素肺炎克雷伯菌菌株。我们研究了这46株肺炎克雷伯菌分离株对头孢菌素的耐药机制。对这些分离株产生的β-内酰胺酶进行等电聚焦分析、检测各种A类、B类和C类β-内酰胺酶的聚合酶链反应以及β-内酰胺酶结构基因序列的测定结果表明，这些分离株大多具有各种类型的广谱β-内酰胺酶。在这46株分离株中，2株产生CMY-2β-内酰胺酶，41株产生DHA-1β-内酰胺酶。41株DHA-1β-内酰胺酶产生菌中的40株同时产生SHV-12超广谱β-内酰胺酶（ESBL），其余1株同时产生SHV-27。此外，1株DHA-1和SHV-12β-内酰胺酶产生菌还产生IMP-1β-内酰胺酶。另一株分离株唯一的广谱β-内酰胺酶是IMP-1。使用XbaI进行的染色体DNA限制性片段分析表明，DHA-1和SHV-12β-内酰胺酶产生菌引起的医院感染在两个中心发生。这是日本首例关于产DHA-1β-内酰胺酶肺炎克雷伯菌包括其他质粒编码的AmpCβ-内酰胺酶引起医院感染的报道。46株分离株中44株对头孢菌素和头孢霉素的耐药机制是ESBL产生和/或质粒编码的AmpCβ-内酰胺酶和/或IMP-1β-内酰胺酶产生。对于2株分离株，其耐药机制无法确定。这些结果表明，有必要尽量减少这些耐药菌株的流行，因为如果临床环境中产生这些广谱β-内酰胺酶的微生物增加，将是一个非常严重的问题。尽早检测到这些菌株并尽早进行严格的感染控制很重要。
