Laing F P, Ramotar K, Read R R, Alfieri N, Kureishi A, Henderson E A, Louie T J
Faculty of Medicine, University of Calgary, Alberta, Canada.
J Clin Microbiol. 1995 Mar;33(3):513-8. doi: 10.1128/jcm.33.3.513-518.1995.
Between April 1992 and December 1993, 80 Xanthomonas maltophilia isolates were collected from 63 patients in three acute-care hospitals in Calgary, Alberta, Canada. On the basis of Centers for Disease Control and Prevention definitions, 48 patients had nosocomial and 15 had community-acquired X. maltophilia. Thirty-eight of the patients were colonized and 25 were infected. Sixty-four percent of patients who acquired X. maltophilia in the intensive care unit (ICU) became infected, whereas 32% of patients in a non-ICU setting became infected. ICU patients tended to be hospitalized for a shorter period of time than non-ICU patients before the onset of X. maltophilia infection. Regardless of being colonized or infected, all patients had debilitating conditions, with respiratory disease being the most common underlying illness (35%). Forty-two patients (88%) with hospital-acquired X. maltophilia received prior antibiotic therapy which included gentamicin, tobramycin, ceftazidime, piperacillin, and imipenem. Agar dilution MICs showed that patient isolates were resistant to these antimicrobial agents that patients had received. Pulsed-field gel electrophoresis of SpeI-digested genomic DNA revealed that six epidemiologically linked patient isolates from the ICU of one acute-care hospital had identical DNA profiles. In contrast, isolates from patients from the other two hospitals had unique genotype profiles (n = 57) regardless of the presence or absence of an epidemiologic association. In these patients there was genetic evidence against the acquisition of a resident hospital clone. These results indicate that pulsed-field gel electrophoresis can resolve genotypically distinct strains of X. maltophilia and, consequently, is a useful tool for evaluating nosocomial infections caused by X. maltophilia.
1992年4月至1993年12月期间,从加拿大艾伯塔省卡尔加里市的三家急症医院的63名患者中收集了80株嗜麦芽窄食单胞菌。根据疾病控制与预防中心的定义,48例患者发生医院感染,15例患者发生社区获得性嗜麦芽窄食单胞菌感染。38例患者为定植,25例患者为感染。在重症监护病房(ICU)获得嗜麦芽窄食单胞菌的患者中有64%发生感染,而在非ICU环境中的患者中有32%发生感染。在嗜麦芽窄食单胞菌感染发作前,ICU患者的住院时间往往比非ICU患者短。无论定植或感染,所有患者均有衰弱性疾病,其中呼吸系统疾病是最常见的基础疾病(35%)。42例(88%)医院获得性嗜麦芽窄食单胞菌感染患者接受过包括庆大霉素、妥布霉素、头孢他啶、哌拉西林和亚胺培南在内的抗生素治疗。琼脂稀释法测定的最低抑菌浓度显示,患者分离株对这些患者接受过的抗菌药物耐药。对经SpeI酶切的基因组DNA进行脉冲场凝胶电泳分析显示,一家急症医院ICU的6株在流行病学上相关的患者分离株具有相同的DNA图谱。相比之下,来自其他两家医院患者的分离株(n = 57)具有独特的基因型图谱,无论是否存在流行病学关联。在这些患者中,有基因证据表明未获得医院固有克隆。这些结果表明,脉冲场凝胶电泳可分辨嗜麦芽窄食单胞菌在基因型上不同的菌株,因此是评估嗜麦芽窄食单胞菌引起的医院感染的有用工具。