Monoclonal antibodies have been raised to components on the surface of glutaraldehyde-fixed zoospores and cysts of an isolate of the pathogenic fungus Phytophthora cinnamomi. Hybridoma supernatants were screened using an immunofluorescence assay, and of 35 cell lines producing antibodies that reacted with the P. cinnamomi cells, 10 have been selected and their specificities examined in detail. The monoclonal antibodies were found to possess a valuable spectrum of taxonomic specificities, and have revealed, for the first time, the presence of isolate-specific antigens on the surface of P. cinnamomi cells. The monoclonal antibodies were tested against six isolates of P. cinnamomi, six species of Phytophthora, and three species of Pythium. In addition to the isolate-specific monoclonal antibodies, species-specific and genus-specific markers which are unambiguous in tests conducted so far have been obtained. The monoclonal antibodies have also revealed the presence of spatially restricted antigens on the surface of the zoospores. Some of these segregated antigens are species-specific and others are more general, occurring in all Phytophthora and Pythium species examined. All of the monoclonal antibodies promise to be of great assistance in investigations of the biology and taxonomy of P. cinnamomi. The methods described should be readily applicable to studies of other fungal pathogens.

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SUMMARY The role of ascitic fluid collagen in the pathogenesis of the coagulopathy that follows peritoneovenous shunting was examined. Collagen was partially purified from ascitic fluid and infused into rabbits. All animals developed changes in their haemostatic profile consistent with intravascular coagulation. Aspirin therapy, for five days before the collagen infusion, prevented these changes. Seven patients undergoing a total of eight peritoneovenous shunts for intractable ascites received antiplatelet therapy (aspirin and dipyridamole) in the immediate pre-and postoperative period. After six shunts no thrombocytopenia or prolongation of clotting times developed to suggest decompensated consumptive coagulopathy. Complicating factors may have contributed to the deterioration in haemostasis in the other two patients. There was no early shunt occlusion. The results support the hypothesis that ascitic fluid collagen is important in the pathogenesis of intravascular coagulation postascitic fluid infusion and indicate that antiplatelet drugs may be of value in preventing this complication.Disseminated intravascular coagulation invariably follows the insertion of peritoneovenous (Le Veen) shunts. 1-3 The coagulopathy is clinically significant in 20-50% of patients and often necessitates ligation of the shunt.I 2 4 Although procoagulants, particularly thromboplastin, were considered major mediators of this complication,5 6 the failure of other studies to detect such substances in ascitic fluid7 8 suggested that alternative factors were involved. It has been recently shown that ascitic fluid contains a platelet aggregating factor identified as being collagen.8 It was suggested that this material, by activating both platelets and clotting factors, could be aetiologically significant in the pathogenesis of disseminated intravascular coagulation complicating pentoneovenous shunts.The aim of this study was to confirm that the infusion of collagen purified from ascitic fluid caused disseminated intravascular coagulation in experimental animals, and examine the effects of aspirin

Results of investigations of the factor VIII (FVIII) of a patient with an unusual variant form of von Willebrand's disease (vWD) are presented. A two-peak crossed-immunoelectrophoresis (CIE) pattern was seen when fresh plasma was electrophoresed, but the CIE pattern became normal by incubating the plasma at 37 degree C for more than 72 hr. The two peaks on CIE were separated by cryoprecipitation: the slow-moving peak precipitating and the fast-moving forms of FVIII remaining in the cryosupernate. An additional protein band was seen on multimeric analysis of FVIII. The platelet-rich plasma (PRP) from this patient did not respond to ristocetin, but agglutinated normally in response to botrocetin. Multimeric and CIE analysis of the FVIII post agglutination and 125I-FVIII binding studies to normal formalin-fixed platelets indicated that this patient's FVIII interacted normally with botrocetin but failed to interact with ristocetin. These data strongly suggest that the sites on the FVIII molecule or the multimeric forms involved for ristocetin and botrocetin are different and that the ristocetin reaction is more closely aligned to the physiologic function of FVIII.

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Summary. Twenty‐four amniotic fluid samples were examined for their effects on human platelets. All samples caused irreversible platelet aggregation. The active material precipitated with high‐speed ultracentrifugation and was completely inhibited by prior incubation with purified collagenase. The presence of free collagen in amniotic fluid was further confirmed by polyacrylamide‐gel electrophoresis and hydroxyproline assays. Beside platelet‐aggregating activity, amniotic fluid samples were also shown to significantly shorten the recalcification time of normal plasma. This procoagulant activity appears to be related to the presence of thromboplastin, collagen and other as yet unidentified procoagulant material in amniotic fluid. The presence of activators of platelets and clotting factors in amniotic fluid would account for the strong clotpromoting activity of this fluid. These studies suggest that the ideal management of the coagulopathy of pregnancy should include a combination of anticoagulant and antiplatelet drugs.

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