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Host-pathogen interactions in Streptococcus pyogenes infections, with special reference to puerperal fever and a comment on vaccine development.

  • Thomas Areschoug
  • Fredric Carlsson
  • Margaretha Stålhammar-Carlemalm
  • Gunnar Lindahl
Publishing year: 2004
Language: English
Pages: 9-14
Publication/Series: Vaccine
Volume: 22 Suppl 1
Issue: Suppl 1
Document type: Journal article
Publisher: Elsevier

Abstract english

Streptococcus pyogenes (group A streptococcus) causes a variety of diseases, including acute pharyngitis, impetigo, rheumatic fever and the streptococcal toxic shock syndrome. Moreover, S. pyogenes was responsible for the classical example of a nosocomial infection, the epidemics of puerperal fever (childbed fever) that caused the death of numerous women in earlier centuries. The most extensively studied virulence factor of S. pyogenes is the surface M protein, which inhibits phagocytosis and shows antigenic variation. Recent data indicate that many M proteins confer phagocytosis resistance because the variable N-terminal region has non-overlapping sites that specifically bind two components of the human immune system, the complement inhibitor C4b-binding protein (C4BP) and IgA-Fc. Concerning puerperal fever, molecular and epidemiological analysis suggests that the S. pyogenes surface protein R28 may have played a pathogenetic role in these epidemics. This article summarizes the properties of M protein and the R28 protein and considers a potential problem encountered in connection with the use of animal models for vaccine development.


  • Microbiology in the medical area
  • C4b-binding protein
  • Group A streptococcus
  • Puerperal fever
  • Vaccines
  • IgA-Fc


  • ISSN: 1873-2518
E-mail: fredric [dot] carlsson [at] biol [dot] lu [dot] se

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