Streptococcus suis is a zoonotic pathogen of swine involved in arthritis, polyserositis, and meningitis. Colonization of piglets by S. suis is very common and occurs early in life. The clinical outcome of infection is influenced by the virulence of the S. suis strains and the immunity of the animals. Here, the role of innate immunity was studied in cesarean-derived colostrum-deprived piglets inoculated intranasally with either virulent S. suis strain 10 (S10) or non-virulent S. suis strain T15. Colonization of the inoculated piglets was confirmed at the end of the study by PCR and immunohistochemistry. Fever (≥40.5 °C) was more prevalent in piglets inoculated with S10 compared to T15 at 4 h after inoculation. During the 3 days of monitoring, no other major clinical signs were detected. Accordingly, only small changes in transcription of genes associated with the antibacterial innate immune response were observed at systemic sites, with S10 inducing an earlier response than T15 in blood. Local inflammatory response to the inoculation, evaluated by transcriptional analysis of selected genes in nasal swabs, was more sustained in piglets inoculated with the virulent S10, as demonstrated by transcription of inflammation-related genes, such as IL1B, IL1A, and IRF7. In contrast, most of the gene expression changes in trachea, lungs, and associated lymph nodes were observed in response to the non-virulent T15 strain. Thus, S. suis colonization in the absence of systemic infection induces an innate immune response in piglets that appears to be related to the virulence potential of the colonizing strain.

Streptococcus suis is a Gram-positive opportunistic pathogen causing systemic disease in piglets around weaning age. The factors predisposing to disease are not known. We hypothesized that the tonsillar microbiota might influence disease risk via colonization resistance and/or co-infections. We conducted a cross-sectional case–control study within outbreak farms complemented by selective longitudinal sampling and comparison with control farms without disease occurrence. We found a small but significant difference in tonsil microbiota composition between case and control piglets (n=45+45). Variants of putative commensal taxa, including Rothia nasimurium, were reduced in abundance in case piglets compared to asymptomatic controls. Case piglets had higher relative abundances of Fusobacterium gastrosuis, Bacteroides heparinolyticus and uncultured Prevotella and Alloprevotella species. Piglets developing disease post-weaning had reduced alpha diversity pre-weaning. Despite case–control pairs receiving equal antimicrobial treatment, case piglets had a higher abundance of antimicrobial resistance genes conferring resistance to antimicrobial classes used to treat S. suis. This might be an adaption of disease-associated strains to frequent antimicrobial treatment.

Glaesserella (Haemophilus) parasuis, an early colonizer of the nasal cavity in piglets, is a highly heterogeneous species, comprising both commensal and virulent strains. Virulent G. parasuis strains can cause fibrinous polyserositis called Glässer’s disease. Colostrum is a source of passive immunity for young piglets. When vaccinating sows, protective antibodies are transferred to their offspring through the colostrum. Here, sow vaccination was performed with a protein fragment, F4, from the outer membrane trimeric autotransporters VtaAs exclusively found in virulent G. parasuis. Piglets were allowed to suckle for 3 weeks, following which a challenge with two virulent strains of G. parasuis was performed. A group of nonvaccinated sows and their piglets were included as a control. Antibodies against F4 were confirmed using ELISA in the vaccinated sows and their offspring before the G. parasuis challenge. Compared to the control group, F4-vaccination also resulted in an increased level of serum TGF-β both in vaccinated sows and in their offspring at early time points of life. After the challenge, a lower body temperature and a higher weight were observed in the group of piglets from vaccinated sows. One piglet from the non-vaccinated group succumbed to the infection, but no other significant differences in clinical signs were noticed. At necropsy, performed 2 weeks after the virulent challenge, the level of surfactant protein D (SP-D) in bronchoalveolar lavage was higher in the piglets from vaccinated sows. Vaccination did not inhibit the nasal colonization of the piglets by the challenge strains.

Streptococcus ruminantium is a recent reclassification of the former Streptococcus suis serovar 33. Although knowledge about S. suis is extensive, information on S. ruminantium host range and pathogenic potential is still scarce. This bacterium has been isolated from lesions in domestic ruminants, but there are no reports in wild animals. Here, we provide information on lesions associated with S. ruminantium in Pyrenean chamois (Rupicapra pyrenaica) and domestic sheep from NE Spain, as well as phenotypic biopatterns and antimicrobial resistance (AMR) of the isolates. Overall, lesions caused by S. ruminantium were similar to those caused by S. suis, excluding polyserositis. Heterogeneity of the phenotypic profiles was observed within the S. ruminantium strains by VITEK-2, resulting in only two tests common to all S. ruminantium isolates and different from S. suis: Alpha-Galactosidase and Methyl-B-D-Glucopyranoside, both positive for S. suis and negative for S. ruminantium strains. Isolates from Pyrenean chamois were susceptible to all antimicrobials tested, except danofloxacin, whereas the domestic sheep isolate was resistant to tetracycline. In conclusion, S. ruminantium can cause infection and be associated with pathology in both wild and domestic ruminants. Due to its phenotypic diversity, a specific PCR is optimal for identification in routine diagnosis.