Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis.
Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis.
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DOI：
10.1038/ncomms7740
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发表时间：
2015-03-31
影响因子：
16.6
通讯作者：
Maskell, Duncan J.
中科院分区：
文献类型：
--
作者：
Weinert, Lucy A.;Chaudhuri, Roy R.;Wang, Jinhong;Peters, Sarah E.;Corander, Jukka;Jombart, Thibaut;Baig, Abiyad;Howell, Kate J.;Vehkala, Minna;Valimaki, Niko;Harris, David;Tran Thi Bich Chieu;Nguyen Van Vinh Chau;Campbell, James;Schultsz, Constance;Parkhill, Julian;Bentley, Stephen D.;Langford, Paul R.;Rycroft, Andrew N.;Wren, Brendan W.;Farrar, Jeremy;Baker, Stephen;Ngo Thi Hoa;Holden, Matthew T. G.;Tucker, Alexander W.;Maskell, Duncan J.
猪链球菌在世界范围内引起猪的疾病，并且越来越多地与东亚和东南亚的人畜共患病有关。了解S.猪，我们研究了来自英国和越南的猪和人类的375株具有详细临床表型的分离株的基因组。在这里，我们表明，与疾病相关的分离株包含的基因比非临床分离株少得多，但更有可能编码毒力因子。人类疾病分离株仅限于单一毒力种群，起源于20世纪20年代，当时猪生产得到加强，但没有观察到猪和人分离株之间一致的基因组差异。不同S.猪链球菌亚群中，该细菌经历了高重组率，这意味着世界上任何地方毒力的增加都可能在短时间内产生全球影响。 猪链球菌引起猪的呼吸道感染和人类的脑膜炎。在这里，作者表明，人类疾病分离株仅限于一个单一的毒性种群，并发现猪和人分离株之间没有一致的基因组差异。
Streptococcus suis causes disease in pigs worldwide and is increasingly implicated in zoonotic disease in East and South-East Asia. To understand the genetic basis of disease in S. suis, we study the genomes of 375 isolates with detailed clinical phenotypes from pigs and humans from the United Kingdom and Vietnam. Here, we show that isolates associated with disease contain substantially fewer genes than non-clinical isolates, but are more likely to encode virulence factors. Human disease isolates are limited to a single-virulent population, originating in the 1920, s when pig production was intensified, but no consistent genomic differences between pig and human isolates are observed. There is little geographical clustering of different S. suis subpopulations, and the bacterium undergoes high rates of recombination, implying that an increase in virulence anywhere in the world could have a global impact over a short timescale. The bacterium Streptococcus suis causes respiratory tract infections in pigs and meningitis in humans. Here, the authors show that human disease isolates are limited to a single virulent population and find no consistent genomic differences between pig and human isolates.
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