Molecular epidemiology of endemic Clostridium difficile infection and the significance of subtypes of the United Kingdom epidemic strain (PCR ribotype 1)
Molecular epidemiology of endemic Clostridium difficile infection and the significance of subtypes of the United Kingdom epidemic strain (PCR ribotype 1)
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DOI：
10.1128/jcm.43.6.2685-2696.2005
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发表时间：
2005-06-01
影响因子：
9.4
通讯作者：
Wilcox, MH
中科院分区：
文献类型：
--
作者：
Fawley, WN;Parnell, P;Wilcox, MH
我们之前在我们的机构中鉴定了流行菌株艰难梭菌 PCR 核糖型 1 的两种亚型，一种克林霉素敏感菌株（任意引物 PCR [AP-PCR] Ia 型）和一种密切相关的克林霉素耐药菌株（AP-PCR Ib 型）。我们在两间老年急症内科病房（A病房和B病房）搬迁后立即开展了为期4年的前瞻性流行病学监测，以确定流行的艰难梭菌PCR核糖分型1组亚型的临床流行病学。为了最大限度地提高菌株区分的机会，我们使用了三种 DNA 指纹识别方法：AP-PCR、核糖间隔 PCR (RS-PCR) 和脉冲场凝胶电泳 (PFGE)，来分析从有症状患者和重复环境采样中回收的艰难梭菌分离株。在 B 病房，艰难梭菌感染的发生率与环境中艰难梭菌的患病率显着相关，无论是在与患者和医护人员密切相关的病区（r = 0.53；P < 0.05）还是在高接触点（r = 0.85；P < 0.05）。在病房 A 中未发现这种关系。共鉴定出 17 种不同的艰难梭菌基因型，其中 AP-PCR 鉴定出 17 种，PFGE 鉴定出 12 种，RS-PCR 鉴定出 11 种，但 17 种基因型中只有 4 种引起患者感染。从医院病房环境中回收的分离株更加多样化（14 种基因型）。 AP-PCR类型1a代表>90%的艰难梭菌分离株。除了该基因型之外，从患者粪便和环境表面仅分离出另外两种基因型。 AP-PCR Ib 型（克林霉素抗性 PCR 核糖型 1 克隆）与任何艰难梭菌感染病例均无关，仅在本研究 5 个月前曾与 6 例艰难梭菌感染有关，仅两次从环境中分离出来。该菌株的消失意味着该菌株和密切相关的、广泛分布的艰难梭菌AP-PCR 1a型菌株可能存在毒力和/或选择压力的差异。我们的研究结果强调需要了解临床上重要菌株的流行病学和毒力，以确定艰难梭菌感染的成功控制措施。
We previously identified two subtypes of the epidemic strain Clostridium difficile PCR ribotype 1, one clindamycin-sensitive strain (arbitrarily primed PCR [AP-PCR] type Ia) and a closely related clindamycin-resistant strain (AP-PCR type Ib) in our institution. We have now carried out prospective epidemiological surveillance for 4 years, immediately following the relocation of two acute medicine wards for elderly patients (wards A and B), to determine the clinical epidemiology of subtypes of the epidemic C. difficile PCR ribotype 1 group. To maximize the chance of strain discrimination, we used three DNA fingerprinting methods, AP-PCR, ribospacer PCR (RS- PCR), and pulsed-field gel electrophoresis (PFGE), to analyze C. difficile isolates recovered from symptomatic patients and from repeated environmental samplings. On ward B the incidence of C. difficile infection correlated significantly with the prevalence of environmental C. difficile both in ward areas closely associated with patients and health care personnel (r = 0.53; P < 0.05) and in high-reach sites (r = 0.85; P < 0.05). No such relationships were found on ward A. Seventeen distinct C. difficile genotypes were identified, 17 by AP-PCR, 12 by PFGE, and 11 by RS-PCR, but only 4 of 17 genotypes caused patient infection. Isolates recovered from the hospital ward environment were much more diverse (14 genotypes). AP-PCR type la represented > 90% of the C. difficile isolates. In addition to this genotype, only two others were isolated from both patient feces and environmental surfaces. AP-PCR type Ib (clindamycin-resistant PCR ribotype 1 clone) was not associated with any cases of C. difficile infection and was isolated from the environment on only two occasions, after having been implicated in a cluster of six C. difficile infections 5 months before this study. The disappearance of this strain implies that differences in virulence and/or selective pressures may exist for this strain and the closely related, widespread C. difficile AP-PCR type la strain. Our findings emphasize the need to understand the epidemiology and virulence of clinically significant strains to determine successful control measures for C. difficile infections.