Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis. Weinert, L. A., Chaudhuri, R. R., Wang, J., Peters, S. E., Corander, J., Jombart, T., Baig, A., Howell, K. J., Vehkala, M., Valimaki, N., Harris, D., Chieu, T. T. B., Van Vinh Chau, N., Campbell, J., Schultsz, C., Parkhill, J., Bentley, S. D., Langford, P. R., Rycroft, A. N., Wren, B. W., Farrar, J., Baker, S., Hoa, N. T., Holden, M. T. G., Tucker, A. W., & Maskell, D. J. Nature communications, 6:6740, March, 2015.
doi  abstract   bibtex   
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.
@article{weinert_genomic_2015,
	title = {Genomic signatures of human and animal disease in the zoonotic pathogen {Streptococcus} suis.},
	volume = {6},
	issn = {2041-1723 2041-1723},
	doi = {10.1038/ncomms7740},
	abstract = {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.},
	language = {eng},
	journal = {Nature communications},
	author = {Weinert, Lucy A. and Chaudhuri, Roy R. and Wang, Jinhong and Peters, Sarah E. and Corander, Jukka and Jombart, Thibaut and Baig, Abiyad and Howell, Kate J. and Vehkala, Minna and Valimaki, Niko and Harris, David and Chieu, Tran Thi Bich and Van Vinh Chau, Nguyen and Campbell, James and Schultsz, Constance and Parkhill, Julian and Bentley, Stephen D. and Langford, Paul R. and Rycroft, Andrew N. and Wren, Brendan W. and Farrar, Jeremy and Baker, Stephen and Hoa, Ngo Thi and Holden, Matthew T. G. and Tucker, Alexander W. and Maskell, Duncan J.},
	month = mar,
	year = {2015},
	pmid = {25824154},
	pmcid = {PMC4389249},
	keywords = {Animals, Genetic Variation, Genomics, Humans, Streptococcal Infections/microbiology/*veterinary, Streptococcus suis/*genetics/pathogenicity, Sus scrofa, Swine Diseases/*microbiology, Swine/microbiology, United Kingdom, Vietnam, Virulence Factors/genetics},
	pages = {6740},
}

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