Streptococcus suis causes Streptococcosis in Pigs

S. suis has antigens associated with the Streptococcus group Landcefield D but is taxonomically far from other members in this group. This bacterial colony of non motile coccus, facultative anaerobes, is gram-positive with different length chains. S. suis produces α-hemalysis (imperfect hemolysis) on blood agar and negative catalase (Faklam, 2002). This bacterium is spread throughout the world and has 35 serotypes based on capsular antigens (serotypes 1-34 and serotypes ½) (Goyette-Desjardin et al, 2014). But there is still some controversy because serotypes 20, 22, 26, 32, 33 and 34 have been recommended not to be part of the S. suis species. However the number of serotypes that are considered virulent is relatively small and is highly dependent on geographical location. Many studies on the virulence of S. sui stipe 2 have been carried out but are incomplete. So far the polysaccharide capsule is an important virulence factor. However, the presence of encapsulated serotype 2 strains is also known (Fittipaldi et al, 2012). Some proteins such as muramidase product proteins, extracellular factors and suilysin are proteins that are related to virulence for serotype 2 strains isolated in Europe, and Asia but differ from north American strains (Baum CG and Wisselink H, 2006). So far there is no true determinant of its pathogenicity. In fact, serotype 2 strains from different continents are phenotypically and genotically different.

            Most Asian and European strains of the ST1 type are characterized by multilocal and highly virulent sequences. North American serotype 2 strains include ST 25 and ST 28 with lower virulence capacity. Other serotypes such as serotype 3 and serotype ½ on other continents also need attention (Fittipaldi et al, 2011). The mechanism that allows S. suis to quickly spread to nearby herds is unknown. Bacteria can spread systemically from nasofarink causing septicemia and death. The palate and farink tonsils are the portal of potential entry of S. suis into circulation eventually spreading hematogenously or lymphogenically. The survival of this organism in the bloodstream is facilitated by the presence of polysaccharide capsules and cell walls that efficiently inhibit phagocytosis. If S. suis does not cause acute fatal septicemia, bacteria can reach the central nervous system through the mechanism of brain microvascular endothelial cell invasion or through the choroideus plexus epithelium. In the occurrence of septicemia and infection in the central nervous system, it turns out that the excessive inflammation response plays an important role in the pathogenesis of infection (Auger and Gottschalk, 2017). S.suis can be found all over the world on intensive farming. Serotypes 1-9 include serotype ½ representing 70% of isolates originating from pigs recovering from illness in North America where most research has been done. Serotype 2 is generally the most common worldwide but is lower in North America and higher in Asia and some European countries such as France. Serotype 9 is the type most often isolated in other European countries such as Spain, Germany and the Netherlands (Zeng et al, 2018). 

            Most clinically healthy pigs are carriers of various S. suis serotypes, although some are defeated by virulent strains. S.suis colonized piglets from vaginal secretions during the birth process and while breastfeeding (Amass et al, 1997). Sub-clinical carriers as sources of infection for their partners or when they are put together in a weaning post-weaning cage accompanied by a decrease in maternal antibodies. Clinical infections are mainly seen in piglets, 2-5 weeks post weaning and are very rare in nursing or adult pigs. Transmission between herds occurs when there is movement and mixing of healthy-looking carrier pigs. The introduction of highly virulent strains in new herds causes disease in post-wean or growing pigs. . However, in some sub-clinical groups of malignant carrier serotypes can suddenly arise with serious clinical disease with predisposition such as excessive density, poor ventilation, extreme temperature fluctuations, mixing pigs with different age of more than two weeks and the presence of infection along with other pathogens. 

Outbreaks of disease due to S. suis infection are reported to co-occur with porcine reproductive viruses and respiratory syndrome (PRRS) (Fable et al, 2011). S. suis can also be transmitted through vomiting, and flies even though the probability is low. Although S. suis has been isolated from different mammals and bird species, the importance of the reservoir is unknown.

            The earliest clinical sign is fever without being followed by any other clinical presence. Then it continues to become septicemia within a few days if not treated. During this period fever usually fluctuates, anorexia, defression and lameness. In acute events the pigs die with sub-clinical signs. Meningitis is the most prominent picture if the examination is based on a presumptive diagnosis.  Pigs with early stage meningitis will narrow their eyes together and let their ears turn backward. Other neurological symptoms such as depression, incoordination, dog-sitting, if continued will be accompanied by clinical paralysis, paddling, ophistotonos, convulsions and nystagmus (uncontrolled eyeball motion) (Gottschalk and Segura, M). Swelling in the joints and lameness are signs of polyarthritis. Endocarditis is also often found in post-weaning piglets that die suddenly or piglets with clinical dispone and cyanosis. Clinical breathing can be found in several outbreaks but the role of S. suis without the participation of other pathogens is still controversial.