1887

Abstract

O of the main difficulties in establishing suitable models of staphylococcal infection has always been the resistance of the skin to infection, necessitating the use of artificially high inocula. Elek and Conen (1957) and later James and Macleod (1961) overcame this problem by injecting staphylococci subcu-taneously on a cotton suture. The presence of a foreign body potentiated the infection. Noble (1965) made the system more quantitative by using, as a foreign body, a pellet of cotton dust inserted into a wide-bore needle. The cotton dust, with an accurately measured number of staphylococci, could then be expelled subcutaneously with a wire plunger. In this system, virulence was defined on the basis of dermonecrosis at the injection site.

Using this model of staphylococcal infection, Agarwal (1967 and ) was able to show that there was an inverse relationship between the virulence of the staphylococcal strain and the amount of early fluid exudation and leucocyte infiltration. Repeated staphylococcal infection resulted in protection against dermonecrosis, but not against local bacterial multiplication and abscess formation. Anti-inflammatory agents increased the severity of infection. Of particular interest was the finding that some coagulase-negative strains could impede the development of the early acute inflammatory response although they did not produce dermonecrosis. This suggested that the full expression of staphylococcal virulence required both the capacity to suppress local defences in the skin and to produce tissue damage. Hill (1968) showed that a peptido-glycan “aggressin”, which was left as the residue after cell walls from log-phase skin-virulent strains of had been treated with deoxycholate, not only acted as a local anti-inflammatory agent but also increased the virulence of avirulent strains of S. when injected subcutaneously with them. Glynn (1972) suggested that the term “impedin” would be more appropriate for this virulence factor because it did not appear to be directly toxic. The deoxycholate residue (DOCR) was also a potent anti-inflammatory agent when the experimental animal was infected either intravenously or intraperitoneally. Work by Easmon, Hamilton and Glynn (1973) suggested that DOCR acted upon the kinin system by inhibiting the release of kinins. DOCR also impaired leucocyte chemotaxis (Weksler and Hill, 1969).

Loading

Article metrics loading...

/content/journal/jmm/10.1099/00222615-13-4-495
1980-11-01
2021-10-22
Loading full text...

Full text loading...

References

  1. Agarwal D. S. 1967a; Subcutaneous staphylococcal infection in mice. I. The role of cotton-dust in enhancing infection. Br. J. exp. Path 48:436
    [Google Scholar]
  2. Agarwal D. S. 1967b; Subcutaneous staphylococcal infection in mice. II. The inflammatory response to different strains of staphylococci and micrococci. Br. J. exp. Path 48:468
    [Google Scholar]
  3. Agarwal D. S. 1967c; Subcutaneous staphylococcal infection in mice. III. The effect of active and passive immunization and anti-inflammatory drugs. Br. J. exp. Path 48:483
    [Google Scholar]
  4. Asherson G. L., Zembala M. 1976; Suppressor T cells in cell-mediated immunity. Br. med. Bull 32:158
    [Google Scholar]
  5. Berenbaum M. C., Cope W. A., Double J. A. 1973; The effect of microsomal enzyme inhibition on the immunosuppressive and toxic effects of cyclophosphamide. Clin. exp. Immunol 14:257
    [Google Scholar]
  6. Bøe J. 1945; Investigations on the importance of bacterial allergy for the development of cutaneous infections due to staphylococci. Acta derm.-vener., Stockh 26:111
    [Google Scholar]
  7. Dumont F. 1974; Destruction and regeneration of lymphocyte populations in the mouse spleen after cyclophosphamide treatment. Int. Archs Allergy appl Immun 47:110
    [Google Scholar]
  8. Easmon C. S. F., Glynn A. A. 1975a; The role of humoral immunity and acute inflammation in protection against staphylococcal dermonecrosis. Immunology 29:67
    [Google Scholar]
  9. Easmon C. S. F., Glynn A. A. 1975b; Cell-mediated immune responses in Staphylococcus aureus infections in mice. Immunology 29:75
    [Google Scholar]
  10. Easmon C. S. F., Glynn A. A. 1976; Comparison of subcutaneous and intraperitoneal staphylococcal infections in normal and complement-deficient mice. Infect. Immun 13:399
    [Google Scholar]
  11. Easmon C. S. F., Glynn A. A. 1977; Effect of cyclophosphamide on delayed hypersensitivity to Staphylococcus aureus in mice. Immunology 33:767
    [Google Scholar]
  12. Easmon C. S. F., Glynn A. A. 1978; Role of Staphylococcus aureus cell wall antigens in the stimulation of delayed hypersensitivity after staphylococcal infection. Infect. Immun 19:341
    [Google Scholar]
  13. Easmon C. S. F., Glynn A. A. 1979; The cellular control of delayed hypersensitivity to Staphylococcus aureus in mice. Immunology 38:103
    [Google Scholar]
  14. Easmon C. S. F., Hamilton I., Glynn A. A. 1973; Mode of action of a staphylococcal anti-inflammatory factor. Br. J. exp. Path 54:638
    [Google Scholar]
  15. Elek S. D., Conen P. E. 1957; The virulence of Staphylococcus pyogenes for man. A study of the problems of wound infection. Br. J. exp. Path 38:573
    [Google Scholar]
  16. Glynn A. A. 1972; Bacterial factors inhibiting host defence mechanisms. In Symposium of the Society for General Microbiology edited by Smith H., Pearce J. H. Cambridge University Press: Cambridge; vol 22 p 75
    [Google Scholar]
  17. Heczko P. B., Grov A., Oeding P. 1973; In vivo reactions of staphylococcal antigens. 1. Hypersensitivity to Protein A. Acta path, microbiol. scand 81B:731
    [Google Scholar]
  18. Hill M. J. 1968; A staphylococcal aggressin. J. med. Microbiol 1:33
    [Google Scholar]
  19. Hill H. R., Quie P. G., Pabst H. F., Ochs H. D., Clark R. A., Klebanoff S. J., Wedgwood R. J. 1974; Defect in neutrophil granulocyte chemotaxis in Job’s syndrome of recurrent ‘cold’ staphylococcal abscesses. Lancet 2:617
    [Google Scholar]
  20. James R. C., Macleod C. J. 1961; Induction of staphylococcal infections in mice with small inocula introduced on sutures. Br. J. exp. Path 42:266
    [Google Scholar]
  21. Joahnovsky J. 1958; Role of hypersensitivity in experimental staphylococcal infection. Nature, Lond 182:1454
    [Google Scholar]
  22. Johnson J. E. 3rd, Cluff L. E., Goshi K. 1961; Studies on the pathogenesis of staphylococcal infection. I. The effect of repeated skin infections. J. exp. Med 113:235
    [Google Scholar]
  23. Koenig M. G., Melly M. A., Rogers D. E. 1962; Factors relating to the virulence of staphylococci. II. Observations on four mouse pathogenic strains. J. exp. Med 116:589
    [Google Scholar]
  24. Kowalski J. J., Berman D. T. 1971; Immunobiological activity of cell wall antigens of Staphylococcus aureus. Infect. Imm 4:205
    [Google Scholar]
  25. Melly M. A., Duke L. J., Liau D., Hash J. H. 1974; Biological properties of the encapsulated Staphylococcus aureus M. Infect. Immun. 10:389
    [Google Scholar]
  26. Noble W. C. 1965; The production of subutaneous staphylococcal skin lesions in mice. Br. J. exp. Path 46:254
    [Google Scholar]
  27. Panton P. N., Valentine F. C. O. 1929; Staphylococcal infection and re-infection. Br. J. exp. Path 10:257
    [Google Scholar]
  28. Quie P. G., White J. G., Holmes B., Good R. A. 1967; In vitro bactericidal capacity of human polymorphonuclear leucocytes: diminished activity in chronic granulomatous disease of childhood. J. clin. Invest 46:668
    [Google Scholar]
  29. Reif A. E., Allen J. M. V. 1974; The AKR thymic antigen and its distribution in leukemias and nervous tissues. J. exp. Med 120:413
    [Google Scholar]
  30. Taubler J. H. 1968; Staphylococcal delayed hypersensitivity in mice. I. Induction and in vivo demonstration of delayed hypersensitivity. J. Immun 101:546
    [Google Scholar]
  31. Turk J. L., Parker D., Poulter L. W. 1972; Functional aspects of the selective depletion of lymphoid tissue by cyclophosphamide. Immunology 23:493
    [Google Scholar]
  32. Turk J. L., Poulter L. W. 1972; Selective depletion of lymphoid tissue by cyclophosphamide. Clin. exp. Immunol 10:285
    [Google Scholar]
  33. Weksler B., Hill M. J. 1969; Inhibition of leukocyte migration by a staphylococcal factor. J. Bact 98:1030
    [Google Scholar]
http://instance.metastore.ingenta.com/content/journal/jmm/10.1099/00222615-13-4-495
Loading

Most cited this month Most Cited RSS feed

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error