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.
Highlights
IntroductionHuman 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
Streptococcus suis causes disease in pigs worldwide and is increasingly implicated in zoonotic disease in East and South-East Asia
We do not find any genomic differences between human and pig hosts, human disease isolates are limited to a single virulent population whose origin coincided with the first intensification of pig production
Summary
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. S. suis has been responsible for zoonotic outbreaks in China, with high mortality rates associated with a Streptococcal Septic shock-like syndrome[2] Sporadic outbreaks of this kind are a particular public health concern because they represent a major source of emerging disease with potential global consequences. Disease-causing isolates contain substantially fewer genes than non-clinical isolates, but despite this genomic reduction are more likely to have acquired genes encoding known virulence factors. We do not find any genomic differences between human and pig hosts, human disease isolates are limited to a single virulent population whose origin coincided with the first intensification of pig production
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