Surgical infection
Takesue e r ul.' investigated the production of staphylococcal enterotoxin by methicillin-resistant Staphylococcus aureus (MRSA) with respect to coagulase type. A total of 138 strains of MRSA isolated from clinical material in the surgical ward between 1983 and 1990 were studied. Coagulase type IV strains produced enterotoxin A only, whereas those of type I1 were classified into four groups according to enterotoxin production: enterotoxin B-producing strains (32.7 per cent), C-producing strains (29.8 per cent), B-and C-coproducing strains ( 12.5 per cent), and A-and C-coproducing strains (25.0 per cent). Some 90 per cent of organisms isolated from the faeces of patients with MRSA enteritis were enterotoxin A and C coproducers. The contemporaneous nature of MRSA enteritis and isolation of A-and C-coproducing bacteria demonstrated that these strains caused the enteritis. Although enterotoxin C-producing strains and A and C coproducers were simultaneously prevalent in 1990, the former tended to be sensitive whereas the latter were generally resistant to minocycline. Considering the range of antibiotic sensitivities in coagulase type I1 bacteria, it is therefore considered very important for epidemiological purposes to characterize isolates further by enterotoxin typing.
Various toxic factors induced by endotoxin are thought to be involved in the pathogenesis of severe infection. Ono et a1.' examined the role of platelet-activating factor ( P A F ) in these conditions, clinical and experimental studies being conducted on the relationship between PAF and changes in general parameters after surgical infection. In a clinical study, changes in PAF concentration in the blood of seven patients with disseminated intravascular coagulation (DIC ), five with sepsis and two without, were monitored by spectrometry. The mean PAF level in patients with DIC and sepsis was higher than that in those without sepsis. Moreover, in the former the increase in PAF level with time was found to show a negative correlation with the platelet count. Experimentally, the role of PAF in toxic shock and the effect ofan anti-PAF agent and protease inhibitor were investigated. The endotoxin-induced fall in blood pressure was prevented by both the anti-PAF agent and the protease inhibitor. The decrease in platelet count was more significantly inhibited by the anti-PAF agent than by the protease inhibitor but the blood coagulation-fibrinolysis system was more affected by the protease inhibitor.