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Role of fibrinogen-binding adhesin expression in septic arthritis and septicemia caused by Streptococcus agalactiae
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- Jonsson, Ing-Marie, 1949 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
- Pietrocola, G. (författare)
- Speziale, P. (författare)
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- 2005
- 2005
- Engelska.
- Ingår i: J Infect Dis. - 0022-1899. ; 192:8, s. 1456-64
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- BACKGROUND: Streptococcus agalactiae (group B streptococcus) is an important human pathogen that causes neonatal pneumonia, sepsis, septic arthritis, and meningitis, as well as severe infections in immunocompromised adult patients. The streptococci produce several molecules important for virulence. METHODS: We used a murine model of sepsis and septic arthritis to assess the role of FbsA, a fibrinogen-binding adhesin of S. agalactiae as a virulence determinant. NMRI mice were inoculated intravenously with S. agalactiae strains isogenic for the expression of FbsA. RESULTS: Inoculation with wild-type (wt) streptococci resulted in significantly higher mortality, more-pronounced weight decrease, and more-severe arthritis, compared with inoculation with the FbsA mutant isogenic strain. Neither active nor passive immunization with FbsA or FbsA-specific antibodies, respectively, resulted in any protection against subsequent infection with the S. agalactiae wt strain. CONCLUSION: Our results clearly indicate that the expression of FbsA by Streptococcus agalactiae is a significant virulence determinant in septic arthritis and septicemia. However, because blocking of the fibrinogen binding properties did not protect the host against the action of FbsA-expressing streptococci, we believe that the FbsA molecule has some other presently unknown biological in vivo properties.
Nyckelord
- Animals
- Arthritis
- Infectious/*metabolism/microbiology/mortality
- Bacterial Adhesion/*physiology
- Bacterial Proteins/immunology/*physiology
- Carrier Proteins/immunology/*physiology
- Disease Models
- Animal
- Mice
- Sepsis/*metabolism/microbiology
- Streptococcus agalactiae/*pathogenicity/physiology
- Virulence/genetics
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- Göteborgs universitet
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