Figure 1
Figure 1. Changes in complement and coagulation activation markers. Stored timed EDTA-plasma samples from baboons challenged with intravenous 100 ng/kg Stx1 (▲, left; n = 6) or 50 ng/kg Stx2 (●, right; n = 5) were evaluated by ELISA for levels of (A-B) soluble TCC (C5b-9). After toxin, the (C-D) thrombocytopenia, (E-F) steady or increasing fibrinogen levels (% change from T0), and (G-H) increasing d-dimer levels are consistent with development of hemolytic uremic syndrome and AKI in these models. In contrast, bacteremia induced by intravenous challenge with pathogenic E coli (○, A,C,E,G) or attenuated B anthracis (dashed ▪, A), resulted in rapid and robust rises in complement activation accompanied by increased d-dimer and consumption of platelets and fibrinogen, consistent with disseminated intravascular coagulation. Means are plotted with individual animal values to show variability between animals. Significant differences from T0 (mean of each Stx group): *P < .05, **P < .01, ***P < .001.

Changes in complement and coagulation activation markers. Stored timed EDTA-plasma samples from baboons challenged with intravenous 100 ng/kg Stx1 (▲, left; n = 6) or 50 ng/kg Stx2 (●, right; n = 5) were evaluated by ELISA for levels of (A-B) soluble TCC (C5b-9). After toxin, the (C-D) thrombocytopenia, (E-F) steady or increasing fibrinogen levels (% change from T0), and (G-H) increasing d-dimer levels are consistent with development of hemolytic uremic syndrome and AKI in these models. In contrast, bacteremia induced by intravenous challenge with pathogenic E coli (○, A,C,E,G) or attenuated B anthracis (dashed ▪, A), resulted in rapid and robust rises in complement activation accompanied by increased d-dimer and consumption of platelets and fibrinogen, consistent with disseminated intravascular coagulation. Means are plotted with individual animal values to show variability between animals. Significant differences from T0 (mean of each Stx group): *P < .05, **P < .01, ***P < .001.

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