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. 2015 Mar 31:6:6740.
doi: 10.1038/ncomms7740.

Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis

Lucy A Weinert  1 , Roy R Chaudhuri  2 , Jinhong Wang  1 , Sarah E Peters  1 , Jukka Corander  3 , Thibaut Jombart  4 , Abiyad Baig  1 , Kate J Howell  1 , Minna Vehkala  3 , Niko Välimäki  5 , David Harris  6 , Tran Thi Bich Chieu  7 , Nguyen Van Vinh Chau  8 , James Campbell  9 , Constance Schultsz  10 , Julian Parkhill  6 , Stephen D Bentley  6 , Paul R Langford  11 , Andrew N Rycroft  12 , Brendan W Wren  13 , Jeremy Farrar  9 , Stephen Baker  14 , Ngo Thi Hoa  9 , Matthew T G Holden  6 , Alexander W Tucker  1 , Duncan J Maskell  1 ; BRaDP1T Consortium
Collaborators, Affiliations

Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis

Lucy A Weinert et al. Nat Commun. .

Erratum in

  • Erratum: Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis.
    Weinert LA, Chaudhuri RR, Wang J, Peters SE, Corander J, Jombart T, Baig A, Howell KJ, Vehkala M, Välimäki N, Harris D, Chieu TT, Chau NV, Campbell J, Schultsz C, Parkhill J, Bentley SD, Langford PR, Rycroft AN, Wren BW, Farrar J, Baker S, Hoa NT, Holden MT, Tucker AW, Maskell DJ; BRaDP1T Consortium. Weinert LA, et al. Nat Commun. 2015 May 12;6:7272. doi: 10.1038/ncomms8272. Nat Commun. 2015. PMID: 25966020 Free PMC article. No abstract available.
  • Publisher Correction: Genomic signatures of human and animal disease in the zoonotic pathogen Streptococcus suis.
    Weinert LA, Chaudhuri RR, Wang J, Peters SE, Corander J, Jombart T, Baig A, Howell KJ, Vehkala M, Välimäki N, Harris D, Chieu TTB, Van Vinh Chau N, Campbell J, Schultsz C, Parkhill J, Bentley SD, Langford PR, Rycroft AN, Wren BW, Farrar J, Baker S, Hoa NT, Holden MTG, Tucker AW, Maskell DJ; BRaDP1T Consortium. Weinert LA, et al. Nat Commun. 2019 Nov 22;10(1):5326. doi: 10.1038/s41467-019-13138-w. Nat Commun. 2019. PMID: 31757940 Free PMC article.

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.

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Figures

Figure 1
Figure 1. S. suis populations broken down by metadata.
The distribution of (a) serotype, (b) clinical phenotype and (c) country of origin, among the five populations of S. suis that were identified by our Bayesian analysis of population structure. The figures show that there is little genetic structure with regard to the metadata, although a partial exception is population 1, which is dominated by isolates from Vietnam, and serotype 2, and which contains all the zoonotic isolates.
Figure 2
Figure 2. Genomic differences between non-clinical, systemic and respiratory strains.
Discriminant analysis of principal components, applied to 153 S. suis isolates isolated from pigs in the United Kingdom, using SNPs in the core genome, and presence/absence data for genes in the accessory genome. Isolates were classified as non-clinical (isolated from the nasal passage), systemic (disease-causing and isolated from the brain, blood or joints) or respiratory (disease-causing and isolated from the lungs).
Figure 3
Figure 3. Genome size differences in isolates of different clinical phenotype.
The number of genes in 153 S. suis isolates isolated from pigs in the United Kingdom. Isolates were classified as non-clinical (isolated from the nasal passage) n=62, systemic (disease-causing and isolated from the brain, blood or joints) n=52 or respiratory (disease-causing and isolated from the lungs) n=39. Boxes show the medians and upper and lower quartiles; whiskers show the most extreme values within 1.5 times the interquartile range.
Figure 4
Figure 4. Differences in the accessory genome content of 153S. suis isolates isolated from pigs in the United Kingdom.
Isolates were classified as non-clinical (isolated from the nasal passage), systemic (disease-causing and isolated from the brain, blood or joints) or respiratory (disease-causing and isolated from the lungs). (a) Shows a histogram of the relative frequencies of known virulence genes (orange) versus all other genes (blue). For the systemic isolates, ‘relative frequency’ is defined as psys/ptot, where 0<psys<1 is the proportion of systemic isolates in which the gene appears, and ptot is the same quantity for the total 153-isolate data set. (b) Shows the functional categories associated with all accessory genes, as compared with the subset of these genes that are over-represented in each category of isolates (defined as genes whose relative frequency is >2). (c) Shows the presence on known MGEs for the genes shown in (b).
Figure 5
Figure 5. Dated phylogeny of a virulent zoonotic clade of S. suis.
Phylogeny shows 256 isolates of S. suis from virulent population one that contains all of the zoonotic isolates. Terminal branches are coloured according to the country and host from which the isolate was obtained, and indicate some genetic structuring by country, but little clustering by host. The phylogeny is a Maximum Clade Consensus tree, estimated from an expanded core genome, with MGEs and recombinant sites removed. The clade denoted with an asterisk corresponds to the isolates shown in the right hand peak of Fig. 6.
Figure 6
Figure 6. No genomic differences between isolates from human and pig hosts in Vietnam.
Discriminant Analysis of Principal Components, applied to 191 isolates isolated from human and pig hosts in Vietnam, using SNPs in the core genome, and presence/absence data for genes in the accessory genome. Shown is the first linear discriminant function, and the lack of separation between the distributions suggests a lack of consistent genetic differences between isolates from the two host types.
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References

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