Streptococcus suis epidemic strains were responsible for two outbreaks in China and possessed increased pathogenicity which was featured prominently by inducing an excessive inflammatory response at the early phase of infection. To discover the critical genes responsible for the pathogenicity increase of S. suis epidemic strains, the genome-wide transcriptional profiles of epidemic strain SC84 were investigated at the early phase of interaction with BV2 cells. The overall low expression levels of 89K pathogenicity island (PAI) and 129 known virulence genes in the SC84 interaction groups indicated that its pathogenicity increase should be attributed to novel mechanisms. Using highly pathogenic strain P1/7 and intermediately pathogenic strain 89–1591 as controls, 11 pathogenicity increase crucial genes (PICGs) and 38 pathogenicity increase-related genes (PIRGs) were identified in the SC84 incubation groups. The PICGs encoded proteins related to the methionine biosynthesis/uptake pathway and played critical roles in the pathogenicity increase of epidemic strains. A high proportion of PIRGs encoded surface proteins related to host cell adherence and immune escape, which may be conducive to the pathogenicity increase of epidemic strains by rapidly initiating infection. The fact that none of PICGs and PIRGs belonged to epidemic strain-specific gene indicated that the pathogenicity increase of epidemic strain may be determined by the expression level of genes, rather than the presence of them. Our results deepened the understanding on the mechanism of the pathogenicity increase of S. suis epidemic strains and provided novel approaches to control the life-threatening infections of S. suis epidemic strains.

Streptococcus suis, an emerging zoonotic pathogen, is important reservoirs of antibiotic resistance genes that play critical roles in the horizontal transfer of corresponding resistances. In the present study, 656 antibiotic resistance (AR) genes were detected in 154 of 155 genomes of S. suis strains isolated from the nasopharynx of slaughtered pigs and the lungs of diseased pigs in China. The AR genes were clustered into 11 categories, consisting of tetracycline, macrolides, lincosamide, streptogramin, aminoglycoside, trimethoprim, amphenicols, nucleoside, quinupristin/dalfopristin, glycopeptide, and oxazolidinones resistance genes. In order to investigate the transmission patterns of the AR genes, AR genes-associated the mobile genetic elements (MGEs) were extracted and investigated. Twenty ICEs, one defective ICE, one tandem ICE, and ten prophages were found, which mainly carried tetracycline, macrolides/lincosamides/streptogramin (MLS), and aminoglycosides resistance genes. Three types of DNA cargo with AR genes were integrated into specific sites of ICEs: integrative mobilizable elements (IMEs), cis-IMEs (CIMEs), and transposon Tn916. Obvious differences in AR gene categories were found among the three cargo types. IMEs mainly harbored tetracycline and MLS resistance genes. CIMEs mainly carried aminoglycoside resistance genes, while transposon Tn916 carried only the tet (M) gene. Nearly all AR genes in ICEs were carried by IMEs and CIMEs. IMEs were prevalent and were also detected in additional 29 S. suis genomes. The horizontal transfer of IMEs and CIMEs may play critical role in ICE evolution and AR gene transmission in the S. suis population. Our findings provide novel insights into the transmission patterns of AR genes and the evolutionary mechanisms of ICEs in S. suis.

To date, three Streptococcus parasuis strains, BS26, BS27, and NN1, have been isolated from the blood cultures of patients with peritonitis, pneumonia, and arthritis, indicating that S. parasuis is an emerging threat to susceptible people. There is thus an urgent need to further evaluate the pathogenesis of S. parasuis clinical strains in order to design efficient anti-inflammatory strategies. Our previous study demonstrated the capacity of S. parasuis clinical strains to enter the central nervous system (CNS) of infected mice. However, the characteristics and inflammatory mechanism of CNS infections caused by S. parasuis are still non-available. In the present study, we investigated the proportion and time of two clinical S. parasuis strains NN1 and BS26 on infected mice that developed neurological symptoms. The characteristics of histopathological changes and the cerebral immune response in mice with neurological symptoms were analyzed. Furthermore, we evaluated the roles of microglia and astrocytes in the S. parasuis clinical strain-induced cerebral inflammation. Our data indicated that S. parasuis clinical strains possess a high potential to induce cerebral inflammation in susceptible people at the early phase of infection. Our study contributes to increasing the understanding of the pathogenicity of S. parasuis and the inflammatory mechanisms of the brain against infection caused by S. parasuis.