Elevated levels of intestinal inflammation in Clostridium difficile infection associated with fluoroquinolone-resistant C. difficile.
Elevated levels of intestinal inflammation in Clostridium difficile infection associated with fluoroquinolone-resistant C. difficile.
复制标题
与氟喹诺酮耐药艰难梭菌相关的艰难梭菌感染肠道炎症水平升高。
DOI：
10.1016/j.jhin.2009.05.013
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Guerrant,RL
中科院分区：
文献类型：
--
作者：
Pawlowski,SW;Archbald-Pannone,L;Carman,RJ;Alcantara-Warren,C;Lyerly,D;Genheimer,CW;Gerding,DN;Guerrant,RL
艰难梭菌限制性内切酶分析（REA）型BI[聚合酶链反应（PCR）核型027]菌株具有cdtA/cdtB（二元毒素CDT基因）、tcdC缺失18 bp、毒素A和B浓度升高以及氟喹诺酮类药物耐药性，可能是近期观察到的艰难梭菌感染（CDI）发病率、严重程度和死亡率增加的原因。1-4至少自20世纪80年代初以来就存在的历史性BI菌株也含有18bp缺失、cdtA/cdtB和左氧氟沙星耐药，但以前并未与暴发相关。然而，最近的BI菌株已经获得了对莫西沙星和加替沙星的耐药性。5从2002年到2005年，弗吉尼亚大学医院（UVH）的CDI病例数翻了一番，与环丙沙星使用相关的病例增加了（LAP，个人通信）。先前的研究表明，高水平的粪便乳铁蛋白（白细胞和肠道炎症的标志）与中度至重度临床CDI有关。因此，我们的目的是确定在UVH中是否存在BI菌株，以及基因型、菌株类型或莫西沙星耐药模式与乳铁蛋白水平之间是否存在相关性。
The Clostridium difficile restriction endonuclease analysis (REA) type BI [polymerase chain reaction (PCR) ribotype 027] strain, with cdtA/cdtB (genes for binary toxin CDT), an 18 bp tcdC deletion, elevated toxin A and B concentrations, and fluoroquinolone resistance, is possibly responsible for the increased Clostridium difficile infection (CDI) incidence, severity, and mortality observed recently. 1–4 The historic BI strain, present at least since the early 1980s also contained the 18 bp deletion, cdtA/cdtB, and levofloxacin resistance, but has not previously been associated with outbreaks. 5 The recent BI strain, however, has additionally acquired resistance to moxifloxacin and gatifloxacin. 5From 2002 to 2005, the number of cases of CDI at the University of Virginia Hospital (UVH) doubled and cases associated with ciprofloxacin use increased (LAP, personal communication). Previous work showed that high levels of fecal lactoferrin, a marker of leucocytes and intestinal inflammation, were associated with moderate to severe clinical CDI. 6 Therefore, our aim was to determine whether the BI strain was present at UVH, and if there was a correlation between genotype, strain type, or moxifloxacin resistance patterns, and lactoferrin levels.