In vivo Consequences of the Interaction between Antibiotic-damaged Pathogens and Host Animal Defences

  • C. G. Gemmell
Conference paper

Abstract

Streptococcus pyogenes is recognised as an important cause of infection in man and much of its virulence can be attributed to the possession of both structural and soluble antigens. Although the properties of pathogenic bacteria are often studied after in vitro growth, there is evidence that organisms grown in vivo may differ from those grown in vitro [1,2]. Under these circumstances it is conceivable that the host response may be determined by the expression of virulence factors of the pathogen. It is known that S. pyogenes cells can lose some of their normal complement of M antigen during in vitro culture. Only by exposing such cells to human or animal leukocytes [3] can one enrich the numbers of M-positive organisms within a culture. These bacteria are much less susceptible to serum opsonization and subsequent phagocytosis by leukocytes [4,5]. The presence of M protein as a surface “fuzz” prevents the activation of complement by the alternative pathway and renders the streptococcus resistant to phagocytic adherence and ingestion [6].

Keywords

Cholesterol Migration Carbohydrate Cage Agarose 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Beining PR, Kennedy ER (1983) Characteristics of a strain of Staphylococcus aureus grown in vivo and in vitro. J Bacteriol 85: 732–743Google Scholar
  2. 2.
    Finn TM, Arbuthnott JP, Dougan G (1982) Properties of Escherichia coli grown in vivo using a chamber implant system. J gen Microbiol 128: 3083–3091PubMedGoogle Scholar
  3. 3.
    Becker CG (1967) Enhancing effect of type-specific anti-streptococcal antibodies on the emergence of streptococci rich in M protein. Proc Soc Exp Biol Med 124: 331–335PubMedGoogle Scholar
  4. 4.
    Bisno AL (1979) Alternate complement pathway activation by Group A streptococci: role of M protein. Infect Immun 25: 1172–1176Google Scholar
  5. 5.
    Fox EN (1974) M proteins of Group A streptococci. Bacteriol Rev 38: 57–86PubMedGoogle Scholar
  6. 6.
    Swanson J, Hsu KC, Gotschlich EC (1968) Electron microscopy studies on streptococci. I.M antigen. J Exp Med 130: 1063–1091CrossRefGoogle Scholar
  7. 7.
    Gemmell CG, Peterson PK, Schmeling D, Kim Y, Mathews J, Wannamaker L, Quie PG (1981) Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin. J Clin Invest 67: 1249–1256PubMedCrossRefGoogle Scholar
  8. 8.
    Gemmell CG, Peterson PK, Schmeling D, Quie PG (1982) Studies on the potentiation of phagocytosis of Streptococcus pyogenes by treatment with various antibiotics. Drugs Exptl Clin Res 8: 235–240Google Scholar
  9. 9.
    Nelson RD, Quie PG, Simmons RL (1975) Chemotaxis under agarose: a new and simple method for measuring chemotaxis and spontaneous migration of human polymorphonuclear leukocytes and monocytes. J Immunol 115: 1650–1656PubMedGoogle Scholar
  10. 10.
    Gemmell CG, Amir MKA (1978) Effects of certain antibiotics on the formation of cellular antigens and extracellular products by group A streptococci. IN Pathogenic Streptococci (ed MT Parker) Reedbooks Ltd. England p 67–68Google Scholar
  11. 11.
    Gemmell CG, Amir MKA (1980) Antibiotic induced changes in streptococci with respect to their interaction with human polymorphonuclear leukocytes. IN Current Chemotherapy and Infectious Disease (eds. JD Nelson and C Grassi) Amer Soc Microbiol Washington DC. 2: 810–812Google Scholar
  12. 12.
    Duncan JL (1983) Streptococcal growth and toxin production in vivo. Infect Immun 40: 501–505PubMedGoogle Scholar
  13. 13.
    Knoll H, Holm SE, Gerlach D, Kohler W (1982) Tissue cages for study of experimental streptococcal infection in rabbits. I Production of erythrogenic toxins in vivo. Immunobiology 162: 128–140PubMedGoogle Scholar
  14. 14.
    Amir MKA (1980) Changes in the pathogenicity of streptococci induced by certain antibiotics relevant to the host parasite relationship. PhD Thesis University of GlasgowGoogle Scholar
  15. 15.
    Quie PG, Giebink S, Peterson PK (1981) Bacterial mechanisms for inhibition of ingestion by phagocytic cells. IN Microbial Perturbation of Host Defenses (ed. F O’Grady and H Smith) Acad Press London p 121–141Google Scholar
  16. 16.
    Gemmell CG, O’Dowd A (1984) Regulation of protein A biosynthesis in Staphylococcus aureus by certain antibiotics: its effect on phagocytosis by leukocytes. J Antimicrob Chemother 12: 587–597CrossRefGoogle Scholar
  17. 17.
    Gemmell CG (1978) Effect of subinhibitory concentrations of antibiotics on experimental pyogenic infections in mice. IN Current Chemotherapy (ed.) Amer Soc Microbiol Washington DC p512–514Google Scholar
  18. 18.
    Joiner KA, Gelfand JA, Onderdonk AB, Bartlett JG, Gorbach SL (1980) Host factors in the formation of abscesses. J Infect Dis 142: 40–49PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1985

Authors and Affiliations

  • C. G. Gemmell
    • 1
  1. 1.Department of Bacteriology, Medical SchoolUniversity of Glasgow, Royal InfirmaryGlasgowScotland

Personalised recommendations