Clinical, experimental, and genomic differences between intermediately pathogenic, highly pathogenic, and epidemic...

Area of Science:

• Bacteriology
• Immunology
• Genomics

Background:

• Streptococcus suis outbreaks can cause severe streptococcal toxic-shock-like syndrome (STSLS).
• The pathogenic mechanisms underlying STSLS outbreaks remain largely unknown.

Purpose of the Study:

• To investigate the mechanisms behind the 2005 STSLS outbreak caused by Streptococcus suis.
• To compare the pathogenicity and genomic features of the epidemic ST7 strain with other S. suis strains.

Main Methods:

• Clinical, laboratory, and epidemiological data from 38 S. suis patients were analyzed.
• Experimental infection of mice with S. suis strains ST7, ST1, and ST25 to assess cytokine induction.
• Genomic comparison of ST7 and ST1 with ST25 to identify genetic differences.

Main Results:

• Fourteen of 38 patients presented with STSLS, exhibiting elevated serum levels of key proinflammatory cytokines (IL-1β, IL-6, IL-8, IL-12p70, IFN-γ, TNF-α).
• Mice infected with the epidemic ST7 strain showed significantly higher proinflammatory cytokine levels than those infected with ST1 or ST25.
• Genomic analysis revealed that ST7 acquired additional genomic islands compared to ST1 and ST25, suggesting evolutionary adaptation.

Conclusions:

• The epidemic S. suis ST7 strain evolved from less pathogenic strains (ST25, ST1).
• ST7 possesses a heightened ability to stimulate massive proinflammatory cytokine production, directly leading to STSLS.
• Understanding these evolutionary and pathogenic mechanisms is crucial for controlling S. suis outbreaks.