Transmission of Vibrio cholerae Is Antagonized by Lytic Phage and Entry into the Aquatic Environment
Transmission of Vibrio cholerae Is Antagonized by Lytic Phage and Entry into the Aquatic Environment
复制标题
DOI：
10.1371/journal.ppat.1000187
复制
发表时间：
2008-10-01
期刊：
影响因子：
6.7
通讯作者：
Camilli, Andrew
中科院分区：
文献类型：
--
作者：
Nelson, Eric J.;Chowdhury, Ashrafuzzaman;Camilli, Andrew
霍乱暴发被认为是在由高传染性霍乱弧菌提供动力并通过裂解噬菌体扑灭的爆炸性循环中传播的。然而，缺乏阐明这些因素如何影响传播的研究，因为现场实验几乎是棘手的。其中一个原因是霍乱弧菌在转移到池塘水中后失去了培养能力。这种表型被称为活性但不可培养状态(ABNC；另一个术语是活的但不可培养的)，因为这些细胞维持代谢活动的能力。ABNC细菌可能是暴发的环境宿主，但还没有进行严格的动物研究来验证这一假说。在这个项目中，我们想要确定ABNC细胞与传播的相关性，以及当细菌进入ABNC状态时，裂解噬菌体对霍乱弧菌的影响。在池塘微宇宙中培养自然含有裂解噬菌体或体外衍生霍乱弧菌的米水粪便，并对其可培养能力、感染量和转录组进行了24小时的检测，结果表明，感染的主要因素是可培养的霍乱弧菌，而不是ABNC细胞。由于噬菌体滴度太低，从患者体内脱落后，噬菌体没有立即影响定植。然而，霍乱弧菌在池塘水中孵育24小时后未能在小肠定植，此时噬菌体和ABNC细胞滴度最高。转录分析跟踪了向非传染性ABNC状态的转变，并支持适应营养不良的水生环境的模型。噬菌体对这种适应产生了不可察觉的影响。综上所述，ABNC细胞的增加和裂解噬菌体阻止了传播。因此，如果霍乱弧菌能够在这些负面选择压力在水环境中复合之前快速转移到下一宿主，则具有适应性优势。
Cholera outbreaks are proposed to propagate in explosive cycles powered by hyperinfectious Vibrio cholerae and quenched by lytic vibriophage. However, studies to elucidate how these factors affect transmission are lacking because the field experiments are almost intractable. One reason for this is that V. cholerae loses the ability to culture upon transfer to pond water. This phenotype is called the active but non-culturable state (ABNC; an alternative term is viable but non-culturable) because these cells maintain the capacity for metabolic activity. ABNC bacteria may serve as the environmental reservoir for outbreaks but rigorous animal studies to test this hypothesis have not been conducted. In this project, we wanted to determine the relevance of ABNC cells to transmission as well as the impact lytic phage have on V. cholerae as the bacteria enter the ABNC state. Rice-water stool that naturally harbored lytic phage or in vitro derived V. cholerae were incubated in a pond microcosm, and the culturability, infectious dose, and transcriptome were assayed over 24 h. The data show that the major contributors to infection are culturable V. cholerae and not ABNC cells. Phage did not affect colonization immediately after shedding from the patients because the phage titer was too low. However, V. cholerae failed to colonize the small intestine after 24 h of incubation in pond water-the point when the phage and ABNC cell titers were highest. The transcriptional analysis traced the transformation into the non-infectious ABNC state and supports models for the adaptation to nutrient poor aquatic environments. Phage had an undetectable impact on this adaptation. Taken together, the rise of ABNC cells and lytic phage blocked transmission. Thus, there is a fitness advantage if V. cholerae can make a rapid transfer to the next host before these negative selective pressures compound in the aquatic environment.