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L’hémorragie de Benckiser est un évènement obstétrical grave, secondaire à la rupture d’un vasa praevia dont la fréquence est estimée entre 1/1150 et 1/5000 grossesses. Nous rapportons un cas clinique illustrant les conséquences de la rupture d’un vasa praevia suspecté. Il n’existe pas de recommandation nationale de prise en charge d’un vasa praevia. Les moyens de prévention de l’hémorragie de Benckiser sont détaillés et discutés avec une revue de la littérature.

The ability of deproteinated malaria exoantigens from Plasmodium falciparum (Pf-MT) and P. berghei ANKA (PbA-MT) to activate murine haematopoietic cells was analysed in vitro. Malaria toxins (MT) of both plasmodium species induced cell proliferation and the production of IFN-γ in overnight and long-term (5 days) spleen and bone marrow cultures and a reduction of the number of TNF-α spot forming cells (SFC). When added to cells of malaria-experienced animals, MT decreased the number of IL-4 SPC and increased the number of IL-5 SPC. However, the same proliferative and IFN-γ induction properties as in naive cells were observed. Simultaneous addition of IL-2 and PbA-MT to spleen cells inhibited the proliferation but increased the IFN-γ production usually induced by IL-2. Flow cytometric analysis revealed that the addition of MT triggered an expansion of CD3+ and GR1+ cell populations. Our results suggest that malaria toxins of different species can induce an immediate and strong proliferation and a TH1-type cytokine release by murine cells, independently of previous in vivo priming.

The lack of correlation between parasitaemia and anaemia in severe malaria indicates that factors in addition to schizont rupture or erythrophagocytosis contribute to anaemia. We asked whether malaria toxin (MT) from Plasmodium berghei or P. chabaudi might impair erythropoiesis. Daily intraperitoneal injection of MT into C57BL/6 mice induced a transient reduction of RBC values by 25–30% after about 2 weeks, followed by increased haematopoiesis in the spleen as compared to mice receiving uninfected RBC preparations. There was a 3 (P. berghei) to 8-fold (P. chabaudi) increase of total proliferative activity in the spleen. Flow cytometric analyses showed that this was accompanied by some differentiation of TER-119 positive erythroid cells and of Gr-1 positive myeloid cells. Erythroid and myeloid progenitor cell-derived colony assays confirmed these results and revealed an increase in the number of CFU-E (200-fold), BFU-E (10-fold) and CFU-GM (20-fold) in the spleen of MT treated mice, as compared to controls.

The authors wish to retract the present form of this publication since serious, inadvertent errors occurred in the compilation of the text and figures, part of which (Figs. 2B, 3, 5) were used in the publication ‘Resistance to cerebral malaria in TNF αβ-deficient mice is associated with a reducton of intercellular adhesion molecule-1 up-regulation and T helper type 1 response’ by Rudin et al., Am. J. Pathol. 1997, 150: 257. We apologize for the errors, but wish to state that the conclusions drawn from the experiments with Plasmodium berghei in IFN-γR-deficient mice are correct.