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Clostridium difficile: Emergence of Hypervirulence and Fluoroquinolone Resistance.

机译:艰难梭菌:高毒力和氟喹诺酮耐药性的出现。

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摘要

Clostridium difficile is a well-known cause of sporadic and healthcare-associated diarrhea. Multihospital outbreaks due to a single strain and outbreaks associated with antibiotic selective pressure, especially clindamycin, have been well documented. Severe cases and fatalities from C. difficile are uncommon. The recent global emergence of a hypervirulent strain containing binary toxin (Toxinotype III ribotype 027), with or without deletion in a regulatory gene (tcdC gene), together with high-level resistance to third generation fluoroquinolones, has been associated with increased morbidity and mortality. Although the defective regulatory gene locus is associated with increased toxin production in vitro, the in vivo significance of this mutation and of the binary toxin remains undefined. To date, treatment strategies have not evolved in response to the emergence of this hypervirulaent strain. We provide a critical, quantitative summary of the evolving clinical and molecular epidemiology of C. difficilealong with implications relevant to future treatment strategies.
机译:艰难梭菌是引起偶发性和医疗保健相关性腹泻的众所周知原因。由单一菌株引起的多院暴发以及与抗生素选择性压力有关的暴发,尤其是克林霉素,已有大量文献记载。难辨梭状芽孢杆菌的严重病例和死亡并不常见。最近全球出现了一种高毒力菌株,该菌株含有二价毒素(毒素型III核糖型027),在调节基因(tcdC基因)中有无缺失,以及对第三代氟喹诺酮类药物的高水平耐药性,与发病率和死亡率增加相关。尽管缺陷的调节基因基因座与体外毒素产生的增加有关,但是这种突变和二元毒素在体内的意义仍然不确定。迄今为止,尚未针对这种高毒力菌株的出现发展出治疗策略。我们提供了艰难梭菌的临床和分子流行病学发展的关键,定量总结,并涉及与未来治疗策略有关的含义。

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