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).


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