Complement depletion aggravates Staphylococcus aureus septicaemia and septic arthritis

The aim of the study was to assess the role of the complement system in Sta phylococcus aureus arthritis and septicaemia. The murine model of haematoge nously acquired septic arthritis was used, injecting intravenously toxic sh ock syndrome toxin-1 (TSST-1), producing S. aureus LS-1. Complement was dep leted using cobra venom factor (CVF). Evaluation of arthritis was performed clinically and histopathologically. In addition, the effect of complement depletion on the phagocytic activity of leucocytes was assessed in vivo and in vitro. Six days after inoculation of S. aureus the prevalence of arthri tis in decomplemented mice was three-fold higher than that in controls (91% versus 25%). The clinical severity of arthritis at the end of the experime nt, expressed as arthritic index, was 7.3 and 1.9, respectively. These find ings were confirmed by histological index of synovitis as well as of cartil age and/or bone destruction being significantly higher in decomplemented mi ce than in controls (9.8 +/- 1.7 versus 4.9 +/- 1.2, P < 0.05; and 7.9 +/- 1.7 versus 3.0 +/- 0.9, P < 0.05, respectively). Also, the septicaemia-indu ced mortality was clearly higher in decomplemented mice compared with the c ontrols. CVF treatment significantly reduced in vivo polymorphonuclear cell -dependent inflammation induced by subcutaneous injection of olive oil and mirroring the capacity of polymorphonuclear cells (PMNC) to migrate and/or extravasate. Besides, the decomplementation procedure significantly impaire d phagocytic activity of peripheral blood leucocytes in vitro, since the nu mber of phagocytes being able to ingest bacteria decreased by 50% when the cells were maintained in decomplemented serum compared with those in intact serum. The conclusion is that complement depletion aggravates the clinical course of S. aureus arthritis and septicaemia, possibly by a combination o f decreased migration/extravasation of PMNC and an impairment of phagocytos is.